Neurological System

Aim of a neurological history and examination: determine whether a neurological

lesion is local or diffuse; and, to determine the location of the neurological lesion,

based upon 4 areas:

(i) Peripheral nerves

(ii) Spinal Cord

(iii) Posterior Cranial fossa (i.e. brainstem and/or cerebellum)

(iv) Cerebrum (i.e. higher functioning centres)

Summary of the neurological system examination:

(i) History with specific symptoms

Headache, Facial/Neck/Back pain, Dizziness/Vertigo, Hearing and Vision,

Motor, Sensation, Gait, Movement, Speech and Swallowing, Altered mental

state (HPDHMSGSA)

(ii) Observation and Inspection

Face, limbs, trunk, muscles, speech, eyes, etc.

(iii) Cranial Nerves (CNII-CNXII)

(iv) Upper Limb and Lower Limbs

Tone, Power, Reflexes, Sensation (touch, pain and vibration),

Proprioception, RoM

(v) Cerebellar Function (Gait, Balance and Speech)

(vi) Autonomic Function and Disease

(vii) Mini-Mental Examination

Elicit a History from Patients

Headache, back or neck pain

Methodology: SOHCRATES and Prior Experiences/New

Tension Headache:

o Bilateral, sensation of tightness, no other symptoms

Migraine:

o Unilateral headache, preceded by aura, photophobia

o Aura:

Localising: e.g. audio or visual hallucination; loss of speech

and taste, etc.

Non-Localising: e.g. general feeling of apprehension

Cluster Headache:

o Pain over one eye, associated with lacrimation, rhinorrhoea & flushing

of the forehead

o Predominantly in males

Cervical Spondylosis:

o Pain over occiput, neck stiffness

o Definition: degenerative OA of the joints between the spinal vertebrae

or neural foramina

Raised ICP:

o Generalised, worse in morning, drowsiness, vomiting/nausea

o Worse in morning due to less dehydration

Meningitis:

o Generalised, photophobia, fever, neck stiffness

Temporal Arteritis:

o Unilateral, tenderness over temporal artery, blurred vision

Acute sinusitis:

o Pain behind eyes, forehead or cheeks

Subarachnoid Haemorrhage:

o Severe headache, instantaneous

Facial pain

Trigeminal neuralgia

o Neuropathic disorder of one or both CNV

o Extremely painful; nicknamed “suicide disease”

o Incidence: highest in >40y.o. and in women

o Pain associated with the mildest touch or no stimulation at al

o Pathology: possibly associated with compression of the trigeminal

nerve within the cranial cavity; i.e. by the superior cerebellar artery

Temporomandibular arthritis

Glaucoma (usually only in acute-angle glaucoma [genetic mutation, acute

event])

o Optic neuropathy; leading to progressive, irreversible loss of vision

o Pathology: chronic elevation of intra-occular pressure; mechanism or

neuron injury not completely understood

o Incidence: leading cause of blindness in African Americans

o Painless, and often late diagnosis due to the preservation of foveal

vision until the late stages of disease

o Screening via measuring of intraocular pressure and cup:disc ratio

Cluster headache

o Affects 0.1% of the population

o Men > women

o Nickname: “Suicide headache”

o >1year in duration, paroxysmal

Temporal arteritis

Psychiatric disease

Aneurysm of internal carotid or posterior communicating artery

Superior orbital fissure syndrome

Fits, faints or “funny turns”

Epilepsy vs. syncope

Epilepsy:

o Grand Mal Epilepsy: tonic-clonic seizures with loss of consciousness

and generally preceded by an aura; often incontinent and tongue

bitten

o Complex seizures: loss of consciousness

o Simple Seizures: uninhibited consciousness

o Petit Mal Epilepsy: occurs in children, and is characterised by loss of

awareness and staring into space; motor function un-involved

o Generalised vs. Localised (i.e. specific or non-specific components of

the seizure)

Syncope:

o Cardiogenic

o Non-Cardiogenic

TIA:

o Sometimes occur without necessary LOC

o Called “drop attacks”

Hypoglycaemia (sweating, weakness, confusion)

Dizziness or vertigo

Vertigo (true):

o There is actually a sense of motion, usually of the surroundings but

also of the head itself

o Symptoms (severe): nausea, vomiting, pallor, headaches, sweating

Balance disorders

o Central: involving the CNS; include:

TIA’s – most common cause of vertigo in people >40y.o.

Common clinical signs:

Bilateral nystagmus

Symptoms more pronounced

o Peripheral: nerve, muscle, or end-organ; include:

Meniere’s Disease

Vestibular neuronitis (commonest cause of vertigo in people

<40y.o)

Acute labyrinthitis

Ototoxic drugs (e.g. aminoglycoside’s associated with

deafness or tinnitus too)

Acoustic neuroma (benign tumour growth on CNVIII)

Internal auditory artery occlusion

Disturbances of vision, hearing or smell

Vision:

o Diplopia = double vision

o Amblyopia = blurry vision

o Photophobia = light intolerance

Hearing: causes of deafness include:

o Trauma: chronic, e.g. excess volume, iPods; acute, e.g. fracture of

petrous bone

o Tumours: acoustic neuroma

o Vascular: disease of the internal auditory artery, rare.

Gait

Classification of Gait Disorders:

1.Hemiplegia: the foot is plantar flexed and the leg is swung in a lateral arc

2.Spastic paraparesis: scissors gait

3.Parkinson's disease: hesitation in starting

shuffling

freezing

festination

propulsion

retropulsion

4.Cerebellar: a drunken gait which is wide-based or reeling on a narrow

base; the patient staggers towards the affected side if there is a unilateral

cerebellar hemisphere lesion

5.Posterior column lesion: clumsy slapping down of the feet on a broad

base

6.Footdrop: high stepping gait

7.Proximal myopathy: waddling gait

8.Prefrontal lobe (apraxic): feet appear glued to floor when erect, but

move more easily when the patient is supine

9.Hysterical: characterised by a bizarre, inconsistent gait

Loss of Sensation or Motor function in upper and lower limbs

Aim: to determine the location of the lesion

(1) NEURON LEVEL:

o UMN Lesions (Pyramidal weakness, greatest effect on anti-gravity

muscles):

Due to: interruption of a neural pathway at a level above the

anterior horn cell.

Result: INCREASE tone and reflexes; DECREASE power

There is little or no muscle wasting.

o LMN lesions:

Due to: lesion that interrupts the reflex arc between the

anterior horn cell and the muscle.

Result: DECREASE tone and reflexes, DECREASE power

Fasciculation (irregular contractions of small areas of muscle)

may be seen

Muscle wasting is prominent.

(2) NMJ LEVEL:

o Myasthenia Gravis:

Autoimmune disease with antibodies specific for Ach receptors

at the post-synaptic junction

Leads to fluctuating muscle weakness and fatigue

DECREASED power (mainly repetitive movements); NORMAL

tone and reflexes

(3) MUSCLE LEVEL:

o Muscle disease causes weakness in a particular muscle or group of

muscles.

o DECREASED tone; DECREASED or ABSENT reflexes

o There is muscle wasting

(4) OTHER:

o e.g. hysteria

o Causes a non-anatomical pattern of weakness

o NORMAL tone and power; unless there has been prolonged disuse,

normal muscle bulk

o Nerve Entrapment/Peripheral Neuropathy:

Pins and needles in hands & feet

o Carpal Tunnel Syndrome:

Pain and parasthesia in hand and wrist

Disturbances of sphincter control

Seizure

Spinal cord tumour/trauma

Involuntary movements or tremor

Parkinsons disease = resting tremor

Cerebellar disease = intention tremor

Akithesia Motor restlessness; constant semi-purposeful movements of

the arms and legs

Asterixis Sudden loss of muscle tone during sustained contraction of

an outstretched limb

Athetosis Writhing, slow sinuous movements, especially of the hands

and wrists

Chorea Jerky small rapid movements, often disguised by the patient

with a purposeful final movement: e.g. the jerky upward arm

movement is transformed into a voluntary movement to

scratch the head

Dyskinesia Purposeless and continuous movements, often of the face

and mouth; often a result of treatment with major

tranquillizers for psychotic illness

Dystonia Sustained contractions of groups of agonist and antagonist

muscles, usually in flexion or extremes of extension; it

results in bizarre postures

Hemiballismu

s

An exaggerated form of chorea involving one side of the

body: there are wild flinging movements which can injure the

patient (or bystanders)

Myoclonic jerk A brief muscle contraction which causes a sudden

purposeless jerking of a limb

Myokymia A repeated contraction of a small muscle group; often

involves the orbicularis oculi muscles

Tic A repetitive irresistible movement which is purposeful or

semi-purposeful

Tremor A rhythmical alternating movement

Speech and swallowing disturbance

Dysarthria

o Difficulty with articulation

Dysphonia

o Altered quality of the voice with reduction in volume

o Due to vocal cord disease

Dysphasia

o Dominant higher centre disorder in the use of symbols for

communication-language.

o Receptive (Wernicke’s) - difficulty in comprehension

o Expressive (Broca’s) - difficulty in putting words together to make

meaning, nominal

Altered cognition

Past Medical History

meningitis or encephalitis

head or spinal injuries

epilepsy or convulsions

previous operations

sexually transmitted disease (e.g. risk factors for HIV infection or syphilis)

Medications (anticonvulsants, contraceptive pill, antihypertensive agents,

steroids, anticoagulants)

Cardiovascular disease (CAD, peripheral vascular disease, AF)

Social History

Smoking

Occupation

Exposure to toxins

Alcohol

Family History

Neurological disease

Mental health

Risk Factors for cerebrovascular disease

Hypertension

Smoking

Diabetes mellitus

Hyperlipidaemia

AF, bacterial endocarditis, MI

Haematological disease

Family history of stroke

Conduct a systematic physical examination on a patient

1. General observation

2. Cranial Nerve Examination

3. Upper and Lower Limb examination

4. Cerebellar Examination

5. Mini mental state examination

General Observation

Consciousness

Neck Stiffness

o Meningism (Kernig's signe should also be elicited if meningitis is

suspected. Flex each hip in turn, then attempt to straighten the knee

while keeping the hip flexed. This is greatly limited by spasm of the

hamstrings (which in turn causes pain) when there is meningism due

to an inflammatory exudate around the lumbar spinal roots.)

o Parkinson’s = resting tremor

o Cervical spondylitis

o Raised intracranial pressure

o Cervical fusion

Higher Centres and Speech

Handedness (assess likely dominant hemisphere)

Orientation (ask patient name, present location and date)

o Dementia

o Delerium

Speech

o Ask patient to describe the room (promote flowing speech)

o Test comprehension (eg. Touch your chin, then your nose)

o Test repetition (eg. Repeat the phrase “no ifs and or buts”)

o Ask patient to name two objects you point at

Recognise (through conversation rather than formal assessment) and explain

speech abnormalities

Dysphasia

1 Receptive (posterior) dysphasia. This is where the patient cannot

understand the spoken (auditory dysphasia) or written word (alexia). This

condition is suggested when the patient is unable to understand any

commands or questions or to recognise written words in the absence of

deafness or blindness. Speech is fluent but disorganised. It occurs with a

lesion (infarction, haemorrhage or space-occupying tumour) in the dominant

hemisphere in the posterior part of the first temporal gyrus (Wernicke's areaf).

2 Expressive (anterior) dysphasia. This is present when the patient

understands, but cannot answer appropriately. Speech is non-fluent. This

occurs with a lesion in the posterior part of the dominant third frontal gyrus

(Broca's areag). Certain types of speech may be retained by these patients.

These include automatic speech. The patient may be able to recite word

series such as the days of the week or letters of the alphabet. Sometimes

emotional speech may be preserved so that when frustrated or upset the

patient may be able to swear fluently. In the same way the patient may be

able to sing familiar songs while unable to speak the words. It is important to

remember that unless the lesion responsible for these defects is very large

there may be no reduction in the patient's higher intellectual functions,

memory or judgment. Some of these patients may incorrectly be considered

psychotic, because of their disorganised speech.

3 Nominal dysphasia. All types of dysphasia cause difficulty naming objects.

There is also a specific type of nominal dysphasia. Here objects cannot be

named (e.g. the nib of a pen) but other aspects of speech are normal. The

patient may use long sentences to overcome failure to find the correct word

(circumlocution). It occurs with a lesion of the dominant posterior

temporoparietal area. Other causes include encephalopathy or the

intracranial pressure effects of a distinct space-occupying lesion; it may also

occur in the recovery phase from any dysphasia. Its localising value is

therefore doubtful.

4 Conductive dysphasia. Here patients repeat statements and name objects

poorly, but can follow commands. This is thought to be caused by a lesion of

the arcuate fasciculus and/or other fibres linking Wernicke's and Broca's

areas.

Dysarthria

Here there is no disorder of the content of speech but a difficulty with

articulation. It can occur because of abnormalities at a number of levels.

Upper motor neurone lesions of the cranial nerves, extrapyramidal conditions

(e.g. Parkinson's disease) and cerebellar lesions cause disturbances to the

rhythm of speech.

Dysphonia

This is alteration of the sound of the voice, such as huskiness of the voice

with decreased volume. It may be due to laryngeal disease (e.g. following a

viral infection or a tumour of the vocal cord), or to recurrent laryngeal nerve

palsy.

Cranial Nerve Examination

Cranial Nerve I: Olfactory Nerve (not tested routinely)

Anatomy

o Purely sensory nerve. Fibres arise in mucous membrance of nose &

pass through cribriform plate of ethmoid bone to synapse in olfactory

bulb. Olfactory tract runs under frontal lobe & terminates in medial

temporal lobe on the same side

Examination

o External appearance of nose (deformity, rash)

o Nasal vestibule

Testing

o Test each nostril separately with a series of bottles containing familiar

smells (coffee, peppermint, vanilla)

Causes of anosmia

o URTI, smoking, old age, ethmoid tumours, skull fracture, congenital,

meningioma of olfactory groove, post-meningitis

Cranial Nerve II: Optic Nerve

Anatomy

o The optic nerve is not really a nerve but an extension of fibres of the

central nervous system that unites the retinas with the brain. It is

purely sensory, contains about a million fibres and extends for about 5

cm passing through the optic foramen close to the ophthalmic artery

and joining the nerve from the other side at the base of the brain to

form the optic chiasm. The spatial orientation of fibres from different

parts of the fundus is preserved so that fibres from the lower part of

the retina are found in the inferior part of the chiasm and vice versa.

Fibres from the temporal visual fields (the nasal halves of the retinas)

cross in the chiasm, whereas those from the nasal visual fields do not.

Fibres for the light reflex from the optic chiasm finish in the superior

colliculus, whence connections occur with both third nerve nuclei. The

remainder of the fibres leaving the chiasm are concerned with vision,

and travel in the optic tract to the lateral geniculate body. From here

the fibres form the optic radiation and pass through the posterior part

of the internal capsule, finishing in the visual cortex of the occipital

lobe. In their course they splay out so that fibres serving the lower

quadrants course through the parietal lobe, while those for the upper

quadrants traverse the temporal lobe. The result of the decussation of

fibres in the optic chiasm is that fibres from the left visual field

terminate in the right occipital lobe and vice versa.

History

o Reduction in visual acuity

o Sudden loss of vision in one eye: embolus to retina, migraine,

temporal arteritis, optic neuritis, non-arteitic ischaemic optic

neuropathy

o Sudden loss of bilateral vision: bilateral occipital lobe infarction or

trauma, bilateral optic nerve damage, psychotic states, methyl alcohol

poisoning

o Gradual loss of vision: cataracts, old age, acute glaucoma; macular

degeneration; diabetic retinopathy (vitreous haemorrhages); bilateral

optic nerve or chiasmal compression; and bilateral optic nerve

damage-for example, tobacco amblyopia

Examination

o Visual acuity: wearing spectacles (if needed). Use a hand held eye

chart or wall chart. Test each eye separately

o Visual fields: Hold hat pin or pen at arms length. Tell patient to look

directly into your eyes. Test when pin can be seen in peripheral vision.

Pin should be brought into visual field from four main directions & four

diagonals, directly into centre of field of vision

Concentric diminution of the field (tunnel vision) may be

caused by glaucoma; retinal abnormalities such as

chorioretinitis or retinitis pigmentosa; papilloedema; or acute

ischaemia, as with migraine. Normally even a reduced field of

vision widens as objects are moved further away. Tubular

diminution of the visual fields suggests hysteria. There is

always a small area close to the centre of the visual fields

where there is no vision (the blind spot). This is the area where

the optic disc is seen on fundoscopy and is the point where the

optic nerve joins the retina. The blind spot enlarges with

papilloedema.

Central scotomata, or loss of central (macular) vision, may be

due to demyelination of the optic nerve (multiple sclerosis

causes unilateral or asymmetrical bilateral scotomata); toxic

causes, such as methyl alcohol (symmetrical bilateral

scotomata); nutritional causes, such as tobacco or alcohol

amblyopia (symmetrical central or centrocecal scotomata);

vascular lesions (unilateral); and gliomas of the optic nerve

(unilateral).

Total unilateral visual loss is due to a lesion of the optic nerve

or to unilateral eye disease.

Bitemporal hemianopia is due to a lesion that affects the centre

of the optic chiasm, damaging fibres from the nasal halves of

the retinas as they decussate. This will result in loss of both

temporal halves of the visual fields. Causes include a pituitary

tumour, a craniopharyngioma and a suprasellar meningioma.

Binasal hemianopia is very rare and is due to bilateral lesions

affecting the uncrossed optic fibres, such as atheroma of the

internal carotid siphon

Homonymous hemianopia is due to a lesion that damages the

optic tract or radiation, affecting the visual field on the right or

left side. For example, left temporal and right nasal field loss

will occur with a right-sided lesion. The exact nature of the

defect depends on the site of interruption of the fibres. In the

optic tract the defect is usually complete-there is no macular

sparing. In the more posterior optic radiation the macular vision

is usually spared if the cause is ischaemia, but not if a

destructive process such as tumour or haemorrhage is

responsible. The macular cortical area is thought to have some

additional blood supply from the anterior and middle cerebral

arteries.

Homonymous quadrantanopia is loss of the upper or lower

homonymous quadrants of the visual fields. This may be due

to temporal lobe lesions (e.g. vascular lesions or tumours),

which cause upper quadrantanopia, or parietal lobe lesions

(e.g. vascular lesions or tumours), which cause lower

quadrantanopia.

o Pupillary Reflexes: Using a pocket torch, shine the light from the side

into one of the pupils to assess its reaction to light. Inspect both pupils

and repeat this procedure on the other side.

Normally the pupil into which the light is shone constricts

briskly-this is the direct response to light. Simultaneously, the

other pupil constricts in the same way. This is called the

consensual response to light.

Move the torch in an arc from pupil to pupil. If an eye has optic

atrophy or severely reduced visual acuity from another cause,

the affected pupil will dilate paradoxically after a short time

when the torch is moved from the normal eye to the abnormal

eye. This is called an afferent pupillary defect (or the Marcus

Gunn pupillary signs). It occurs because an eye with severely

reduced acuity has reduced afferent impulses so that the light

reflex is markedly decreased. When the light is shone from the

normal eye to the abnormal one the pupil dilates, as reflex

pupillary constriction in the abnormal eye is so reduced that

relaxation after the consensual response dominates.

Cranial Nerves III (oculomotor), IV (trochlear) & VI (abducens): The ocular nerves

Anatomy

o III: Motor function. Nuclei located in periaqueductal gray matter of

midbrain & dorsal to somatic motor nucleus. Emerges from the

midbrain, pierces dura & runs in lateral wall of the cavernous sinus.

Leaves through superior orbital fissure & divides into superior division

& inferior division.

o IV: Somatic motor & proprioreceptor function. Trochlear nucleus

located in periaqueductal grey matter. Emerges from dorsal surface of

midbrain, winds around brainstem, pierces dura & runs along

cavernous sinus, passing through the superior orbital fissure

o VI: Somatic & proprioceptive. Nucleus in pons, emerges from the

brainstem between the pons & medulla & enters pontine cistern,

running alongside basilar artery. Pierces dura & enters orbit through

superior orbital fissure.

Examination

o Pupils: Examines for size, shape, equality & regularity. Look for ptosis

o Accommodation: Ask patient to look into distance & then focus on an

object 30cm in front of their nose. Normally constriction of both pupils.

Abnormalities with a midbrain lesion, ciliary ganglion lesion,

Parinaud’s syndrome

o Eye Movements: Ask patient to look laterally right and left, then up

and down

o Diplopia: early sign of ocular muscle weakness. If 2 images are side

by side, lateral or medial recti responsible. If one above the other,

obliques or superior or inferior recti responsible

o III nerve lesion: complete ptosis, divergent strabismus, dilated pupil,

unreactive to direct light & accommodation. Commonly related to

trauma, or idiopathic, vascular lesions, compressive lesions,

ischaemia or infarction

o IV nerve lesion: paralysis of superior oblique with weakness of

downward & outward movement. Patient may tilt head to opposite

shoulder. Usually idiopathic or related to trauma

o VI nerve lesion: failure of lateral movement, convergent strabismus &

diplopia. Images horizontal & parallel to each other. Caused by traum,

Wernicke’s encephalopathy, idiopathic or related to trauma

o Nystagmus: disturbance of tone between opposing ocular muscles,

causing sudden quick movement back to original position.

Jerky horizontal: vestibular lesion, cerebellar lesion, toxins,

internuclear opthalmoplegia

Jerky vertical: brainstem lesion. Upbeat = midbrain or floor of

4th ventricle. Downbeat = foramen magnum lesion

Pendular nystagmus: retinal or congenital

Cranial Nerve V: Trigeminal Nerve

Anatomy

o Sensory & motor fibres

o Its motor nucleus and its sensory nucleus for touch lie in the pons, its

proprioceptive nucleus lies in the midbrain, while its nucleus serving

pain and temperature sensation descends through the medulla to

reach the upper cervical cord. It is the largest of the cranial nerves.

o leaves the pons from the cerebellopontine angle and runs over the

temporal lobe in the middle cranial fossa. At the petrous temporal

bone the nerve forms the trigeminal (Gasserianw) ganglion and from

here the three sensory divisions arise. The first (ophthalmic) division

runs in the cavernous sinus with the third nerve and emerges from the

superior orbital fissure to supply the skin of the forehead, the cornea

and conjunctiva. The second (maxillary) division emerges from the

infraorbital foramen and supplies skin in the middle of the face and the

mucous membranes of the upper part of the mouth, palate and

nasopharynx. The third and largest (mandibular) division runs with the

motor part of the nerve, leaving the skull through the foramen ovale to

supply the skin of the lower jaw and mucous membranes of the lower

part of the mouth

o Pain and temperature fibres from the face run from the pons through

the medulla as low as the upper cervical cord, terminating in the spinal

tract nucleus as they descend. The second order neurones arise in

this nucleus and ascend again as the ventral trigeminothalamic tract.

Touch and proprioceptive fibres terminate in the pontine or main

sensory and mesencephalic nuclei, respectively, to form the dorsal

and ventral mesencephalic tracts. Because of this segregation in the

brainstem, lesions of the medulla or upper spinal cord can cause a

dissociated sensory loss of the face-loss of pain and temperature

sensation, but retention of touch and proprioception.

o Motor fibres supply muscles of mastication

History

o Pain in distribution of part of trigeminal nerve (trigeminal neuralgia)

o Pontine lesion, compression of trigeminal nerve

o Muscle weakness

Examination

o Corneal reflex: Lightly touch cornea with a wisp of cotton brought to

eye from side. Reflex blinking of both eyes is normal. Ask patient if

they feel cottonwool. Sensory component mediated by ophthalmic

division of 5th nerve, reflex blink mediated by facial nerve innervation

of orbicularis oculi muscles. If blinking occurs with contralateral eye,

indicates an ipsilateral 7th nerve palsy

o Facial Sensation: 3 divisions of nerve (forehead, cheek, jaw)

o Motor division: Wasting of temporal & masseter muscles (ask patient

to clench teeth & palpate). Ask patient to open mouth & hold it open

while you try to shut it. Unilateral lesion of motor division causes jaw to

deviate towards affected side

o Jaw jerk: Normally slight closure of mouth or no reaction at all. UMNL

above pons jaw jerk is greatly exaggerated

Causes

o Central: vascular lesion, tumour, syringobulbia

o Peripheral: aneurysm, tumour, chronic meningitis

Cranial Nerve VII: Facial Nerve

Anatomy

o Nucleus lies in pons next to VI cranial nerve nucleus. Leaves pons

with VII nerve through cerebellopontine angle. After entering the facial

canal it enlarges to become the geniculate ganglion. The branch that

supplies the stapedius muscle is given off from within the facial canal.

The chorda tympani (containing taste fibres from the anterior two-

thirds of the tongue) joins the nerve in the facial canal. The seventh

nerve leaves the skull via the stylomastoid foramen. It then passes

through the middle of the parotid gland and supplies the muscles of

facial expression

History

o Difficulty speaking, keeping liquids in mouth, facial asymmetry in

mirror

o Dryness of eyes or mouth

Examination

o Facial asymmetry: unilateral drooping of corner of mouth, smoothing

of wrinkled forehead & nasolabial fold. Symmetry maintained with

bilateral palsy

o Muscle power: Ask patient to look up (wrinkling of forehead. Relatively

preserved in UMNL) Ask patient to puff out cheeks, shut eyes tightly,

grin, show teeth. In a LMNL all muscles of facial expression are

affected on the side of the lesion. In Bell’s phenomenon with LMNL

palsy, upward movement of eyeball & incomplete closure of eyelid

when shutting eyes

Causes

o UMNL: vascular lesion, tumour

o LMNL: Bell’s palsy (most common) vascular lesion, tumour,

syringobulbia, MS, chronic meningitis, fracture, sarcoidosis

o Bilateral facial weakness: Guillain-Barré syndrome, sarcoid, bilateral

parotid disease, Lyme disease or rarely mononeuritis multiplex

o Unilateral loss of taste: middle ear lesions involving chorda tympani or

lingual nerve (rare)

Cranial Nerve VIII: Acoustic Nerve

Anatomy

o Two components: Cochlear (with afferent fibres subserving hearing) &

vestibular (afferent fibres subserving balance)

o Fibres for hearing originate in organ of Corti & run to cochlear nuclei in

the pons, then there is bilateral transmission to the medical geniculate

bodies & then to superior gyrus of temporal lobes

o Fibres for balance begin in utricle & semicircular canals & join auditory

fibres in facial canal. Enter brainstem at cerevellopontine angle, enter

pons & runs throughout the brainstem & cerebellar

History

o Loss of hearing (mostly unilateral)

o Trauma, exposure to loud noise etc…

Examination

o Look to see if patient is wearing hearing aid, remove it. Examine pinna

(scars), pull on pinna gently (tender = external ear disease of

temporomandibular joint disease). Feel for nodes (pre- & post-

auricular = disease of external auditory meatus)

o Otoscope

o Test Hearing: rub fingers next to ear/whisper numbers (68 tests high

tone. 100 tests low tone)

o Rinne’s Test: 256 Hz vibrating tuning fork placed on mastoid process,

when sound is no longer heard, place in line with external meatus.

Nerve deafness- sound audible at external meatus (air & bone

conduction reduced equally) = Rinne +ve. Conduction deafness- no

note audible at external meatus = Rinne –ve

o Weber’s test: 256 Hz tuning fork positioned on centre of forehead.

Nerve deafness- sound heard better in normal ear. Conduction

deafness- sound louder in abnormal ear

Causes

o Unilateral nerve deafness: tumours, trauma, vascular disease of

internal auditory artery

o Bilateral nerve deafness: environmental exposure to noise,

degeneration, toxicity, infection, Meniere’s disease, brainstem disease

o Conduction deafness: wax, otitis medica, otosclerosis, Paget’s

disease of bone

Causes of vestibular abnormalities

o Labyrinthine causes: motion sickness, streptomycin toxicity, acute

labyrinthitis

o Vestibular causes: vestibular neuronitis

o Brainstem causes: vascular lesions, tumours, demyelination, migraine

o Temporal lobe dysfunction

Cranial Nerves IX (Glossopharyngeal) & X (Vagus)

Anatomy

o Motor, sensory & autonomic functions

o Nerve fibres from nuclei in medulla form multiple nerve rootlets as

they exit the medulla. Join to form IX & X nerves (also contribute to

XI). Nerves emerge from skull through jugular foramen

o IX nerve receives sensory fibres from nasopharynx, pharynx, middle &

inner ear & posterior third of tongue. Carries secretory fibres to parotid

gland.

o X nerve receives sensory fibres from pharynx & larynx. Innervates

muscles of pharynx, larynx & palate

History

o Glossopharyngeal lesion: no definite symptoms. Difficulty in

swallowing dry foods

o Glossopharyngeal neuralgia: tic douloureux. Sudden shooting pains

radiate from one side of throat to ear.

o Unilateral vagus nerve paralysis: difficulty in initiating swallowing of

solids & liquids, hoarseness

Examination

o Ask patient to open mouth & inspect palate with torch (note uvula

displacement)

o Ask patient to say ‘ah’. If uvula drawn to one side, indicates a

unilateral X nerve palsy (drawn to normal side)

o Test gag reflex-pressing a stick into the tonsillar fossa will cause

patient to gag. Ask patient if sensation if comparable on both sides.

(IX sensory component. X motor component)

o Ask patient to speak in order to assess hoarseness (X nerve lesion)

Causes of nerve palsy

o Central: vascular lesions, tumours, syringobulbia, MND

o Peripheral: aneurysms at base of skull, tumours, chronic meningitis,

Guillain-Barre syndrome

Cranial Nerve XI: Accessory Nerve

Anatomy

o Central portion of nerve arises in medulla close to nuclei of IX, X & XII

nerves. Spinal portion arises from upper 5 cervical segments. Leaves

skull with IX & X nerves through jugular foramen. Central division

provides motor fibres to the vagus & spinal division innervates the

trapezius & sternomastoid muscles

Examination

o Stand behind patient

o Ask patient to shrug shoulders (test power of trapezius). Feel bulk &

attempt to push shoulders down

o Place hand on lower jaw, ask patient to rotate head against your

resistance to test power of sternomastoid. Feel bulk of muscle on

opposite side

o Torticollis (overactivity of multiple neck muscles) more common than

weakness

Causes of nerve palsy

o Unilateral: trauma, poliomyelitis, basilar invagination, syringomyelia,

tumours

o Bilateral: MND, poliomyelitis, Guillain-Barre syndrome

Cranial Nerve XII: Hypoglossal Nerve

Anatomy

o Nerve arises from medulla. Leaves skull via the hypoglossal foramen.

Motor nerve for tongue

History

o Difficulty swallowing, sensation of choking

Examination

o Inspect tongue at rest on floor of mouth (wasting, fasciculations =LMN

lesion)

o Ask patient to poke tongue straight out (deviates to weaker side if

there is a unilateral LMN lesion. Unilateral UMN lesion causes no

deviation) Clinically obvious UMN lesion is usually bilateral, results in

small, immobile tongue.

o Pseudobulbar palsy = IX, X & XII nerve palsy

o Assess power by asking patient to push tongue against side of cheek

Causes

o Bilateral UMNL: vascular lesions, MND, tumours

o Unilateral LMNL: vascular lesions, MND, thrombosis of vertebral

artery, syringobulbia. Meningitis, trauma, tumours, lymphadenopathy,

Arnold-Chiari malformation

o Bilateral LMNL: MND, Guillain-Barre syndrome, poliomyelitis, Arnold-

Chiari malformation

o Movement disorders: Parkinson’s (coarse tremor of tongue), athetoid,

choreiform, tardive dyskinesia

Clinical features of pseudobulbar and bulbar palsies

Feature

Pseudobulbar (bilateral UMN

lesions of IX, X and XII)

Bulbar (bilateral LMN

lesions of IX, X and XII)

Gag

reflex

Increased or normal Absent

Tongue Spastic Wasted, fasciculations

Jaw jerk Increased Absent or normal

Speech Spastic dysarthria Nasal

Other Bilateral limb UMN (long tract)

signs

Signs of the underlying cause-

e.g. limb fasciculations

  Labile emotions Normal emotions

Causes Bilateral cerebrovascular disease

(e.g. both internal capsules)

Motor neurone disease

Guillain-Barré syndrome

  Multiple sclerosis Poliomyelitis

  Motor neurone disease Brainstem infarction

Elicit and explain abnormalities of upper and lower limbs

Examination of Upper Limbs

Observation

o Posture, muscle bulk, abnormal movements, fasciculations

Tone

o Rotate elbow + wrists with supination and pronation of the elbow joints

at different rates

o The cogwheel rigidity of Parkinson's disease is an important

abnormality of tone in the upper limbs and should be recognised. It is

best assessed by having the patient move the other arm up and down

as the examiner moves the hand and forearm, testing tone at the wrist

and elbow

Power

Scale

0 Complete paralysis (no movement).

1 Flicker of contraction possible.

2 Movement is possible when gravity is excluded.

3 Movement is possible against gravity but not if any further resistance is

added.

4- Slight movement against resistance.

4 Moderate movement against resistance.

4+ Submaximal movement against resistance.

5 Normal Power

o Shoulder Abduction-mostly deltoid and supraspinatus-(C5, C6): the

patient should abduct the arms with the elbows flexed and resist the

examiner's attempt to push them down.

o Shoulder Adduction-mostly pectoralis major and latissimus dorsi-(C6,

C7, C8): the patient should adduct the arms with the elbows flexed

and not allow the examiner to separate them.

o Elbow Flexion-biceps and brachialis-(C5, C6): the patient should bend

the elbow and pull so as not to let the examiner straighten it out.

o Elbow Extension-triceps brachii-(C7, C8): the patient should bend the

elbow and push so as not to let the examiner bend it

o Wrist Flexion-flexor carpi ulnaris and radialis-(C6, C7): the patient

should bend the wrist and not allow the examiner to straighten it.

o Wrist Extension-extensor carpi group-(C7, C8): the patient should

extend the wrist and not allow the examiner to bend it

o Finger Extension-extensor digitorum communis, extensor indicis and

extensor digiti minimi-(C7, C8): the patient should straighten the

fingers and not allow the examiner to push them down (push with the

side of your hand across the patient's metacarpophalangeal joints).

o Finger Flexion-flexor digitorum profundus and sublimis-(C7, C8): the

patient squeezes two of the examiner's fingers.

o Finger Abduction-dorsal interossei-(C8, T1): the patient should spread

out the fingers and not allow the examiner to push them together.

o Finger Adduction-volar interossei-(C8, T1): the patient holds the

fingers together and tries to prevent the examiner from separating

them further.

Reflexes

Classification

O absent

+ present but reduced

++ normal

+++ increased, possibly normal

++++ greatly increased, often associated with clonus

o Biceps Jerk (C5, C6): place one forefinger on the biceps tendon and

tap with tendon hammer

o triceps jerk (C7, C8), support the elbow with one hand and tap over

the triceps tendon

o Brachioradialis jerk (C5, C6): strike the lower end of the radius above

the wrist

Coordination

o Finger-nose test: ask patient to touch their own nose, then the

examiner’s forefinger, both briskly and slowly. Look for intention

tremor & past-pointing, which occur with cerebellar disease.

o Rapidly alternating movements: ask patient to pronate & supinate their

hand on the dorsum of the other hand rapidly. Slow & clumsy in

cerebellar disease (called dysdiadochokinesis). Also altered in

extrapyramidal & pyramidal disorders

o Rebound: Ask the patient to lift the arms rapidly from the sides and

then stop. Hypotonia due to cerebellar disease causes delay in

stopping the arms.

Sensation

o Pain: Test normal area (such as chest). Begin proximally, then test in

each dermatome. Compare right and left sides

o Temperature: Cold sensation can be tested using a metal object

o Vibration: 128 Hz tuning fork. Ask patient to close eyes then place fork

on one of the distal interphalangeal joints. Deaden fork, patient should

be able to say when vibration stops. Compare one side with other.

Move up to ulnar head, elbows, shoulders if abnormalities

o Proprioception: use distal interphalangeal joint of patient’s little finger.

Move it up and down to demonstrate positions, then ask patient to

close their eyes. If abnormality proceed to wrist & elbows

o Light touch: Touch skin with a wisp of cotton wool. Ask patient to close

eyes & say yes when sensation is felt

o C5 supplies the shoulder tip and outer part of the upper arm; C6

supplies the lateral aspect of the forearm and thumb; C7 supplies the

middle finger; C8 supplies the little finger; T1 supplies the medial

aspect of the upper arm and elbow.

Examination of Lower Limbs

Observation

o Posture, muscle bulk, abnormal movements, fasciculations

Tone

o Test and knees and ankles

o Clonus: sustained rhythmical contraction of the muscles when put

under sudden stretch. Hypertonia from UMNL. Sharply dorsiflex foot

with knee bent & thigh externally rotated. Test for patellar clonus by

resting hand on lower part of quadriceps with knee extended & move

patella down sharply

Power

o Hip Flexion-psoas and iliacus muscles-(L2, L3): ask the patient to lift

up the straight leg and not let you push it down (having placed your

hand above the knee).

o Hip Extension-gluteus maximus-(L5, S1, S2): ask the patient to keep

the leg down and not let you pull it up from underneath the calf or

ankle.

o Hip Abduction-gluteus medius and minimus, sartorius and tensor

fasciae latae-(L4, L5, S1): ask the patient to abduct the leg and not let

you push it in.

o Hip Adduction-adductors longus, brevis and magnus-(L2, L3, L4): ask

the patient to keep the leg adducted and not let you push it out

o Knee Flexion-hamstrings (biceps femoris, semimembranosus,

semitendinosus)-(L5, S1): ask the patient to bend the knee and not let

you straighten it. If there is doubt about the real strength of knee

flexion, it should be tested with the patient in the prone position. Here

possible help from hip flexion is prevented and the muscles can be

palpated during contraction.

o Knee Extension-quadriceps femoris (this muscle is three times as

strong as its antagonists, the hamstrings)-(L3, L4): with the knee

slightly bent, ask the patient to straighten the knee and not let you

bend it.

o Plantar flexion-gastrocnemius, plantaris, soleus-(S1, S2): ask the

patient to push the foot down and not let you push it up.

o Dorsiflexion-tibialis anterior, extensor digitorum longus and extensor

hallucis longus-(L4, L5): ask the patient to bring the foot up and not let

you push it down. The power of the ankle joint can also be tested by

having the patient stand up on the toes (plantar flexion) or on the

heels (dorsiflexion); these movements may also be limited if

coordination is impaired.

o Eversion-peroneus longus and brevis, and extensor digitorum longus-

(L5, S1): ask the patient to evert the foot against resistance.

o Inversion-tibialis posterior, gastrocnemius and hallucis longus-(L5,

S1): with the foot in complete plantar flexion, ask the patient to invert

the foot against resistance

Reflexes

o Knee jerk (L3, L4). Slide one arm under the knees so that they are

slightly bent and supported. The tendon hammer is allowed to fall onto

the infrapatellar tendon. Normally, contraction of the quadriceps

causes extension of the knee.

o Ankle jerk (S1, S2). Have the foot in the mid-position at the ankle with

the knee bent, the thigh externally rotated on the bed, and the foot

held in dorsiflexion by the examiner. The hammer is allowed to fall on

the Achilles tendon. The normal response is plantar flexion of the foot

with contraction of the gastrocnemius muscle.

o Plantar reflex (L5, S1, S2). After telling the patient what is going to

happen, use a blunt object (such as the key to an expensive motor

car) to stroke up the lateral aspect of the sole, and curve inwards

before it reaches the toes, moving towards the middle

metatarsophalangeal (MTP) joint. The patient's foot should be in the

same position as for testing the ankle jerk. The normal response is

flexion of the big toe at the MTP joint in patients over one year of age

Coordination

o Heel-shin test. Ask the patient to run the heel of one foot up and

down the opposite shin at a moderate pace and as accurately as

possible. In cerebellar disease the heel wobbles all over the place,

with oscillations from side to side and overshooting.

o Toe-finger test. Unfortunately, a toe-nose test is not a practical way

of assessing the lower limbs, so a toe-finger test is used. Ask the

patient to lift the foot (with the knee bent) and touch the examiner's

finger with the big toe. Look for intention tremor.

o Foot-tapping test. Rapidly alternating movements are tested by

getting the patient to tap the sole of the foot quickly on the examiner's

hand or tap the heel on the opposite shin. Look for loss of rhythmicity.

Sensation (as for upper limb)

o Pain sensation

o Vibration

o Proprioception (using big toe)

o Light touch

o L2 supplies the upper anterior thigh; L3 supplies the area around the

front of the knee; L4 supplies the medial aspect of the leg; L5 supplies

the lateral aspect of the leg and the medial side of the dorsum of the

foot; S1 supplies the heel and most of the sole; S2 supplies the

posterior aspect of the thigh; S3, S4 and S5 supply concentric rings

around the anus.

Gait

(1) Make sure patient’s legs are clearly visible

(2) Ask patient to walk normally for a few metres, then turn and walk towards you

o Assess how quickly the patient is able to start, and how fast they can

turn around (looking for Parkinsonism)

(3) Ask patient to walk heel to toe

o This will aim to exclude a midline cerebellar lesion

(4) Ask patient to walk on toes

o Excludes an S1 lesion

(5) Ask patient to walk on heels

o Exclude L4 and L5 lesion, and this will cause foot drop

(6) Ask the patient to squat and stand

o This will test for proximal myopathy

(7) Romberg test: ask patient to stand erect with feet together. Ask patient to

stand with eyes open and closed for periods of time. Compare steadiness

o Eyes Closed with increased unsteadiness Proprioceptive

dysfunction

o Eyes Open with increased unsteadiness Cerebellar or vestibular

dysfunction (i.e. balance)

Upper motor neuron lesionLesion has interrupted a neural pathway at a level

above the anterior horn cell: for example, motor pathways in the cerebral cortex,

internal capsule, cerebral peduncles, brainstem or spinal cord.

Weakness in all muscles. Great weakness of abductors and extensors in the

upper limb & flexors & abductors in the lower limb

Muscle wasting slight or absent

Increased tone

Reflex hyperactivity

Affected areas

o Monoplegia: motor cortex or partial internal capsule lesion

o Hemiplegia: lesion affecting projection of pathways from contralateral

motor cortex

o Paraplegia: spinal cord trauma

o Quadriplegia: Spinal cord trauma or brainstem lesion

Causes

o Vascular disease: Lesions in internal carotid artery result in

hemiplegia on opposite side of body. Homonymous hemianopia,

hemianaesthesia & dysphasia may occur. Lesions in vertebrobasilar

artery produce cranial nerve palsies, cerebellar signs, Horner’s

syndrome & sensory loss

o Compressive & infiltrative lesions: Occur in lobes of brain. Focal signs

depend on tumour site

o Demyelinating disease: MS

o Infection: HIV

Lower motor neuron lesion

Lesions interrupt the spinal reflex arc (occur in spinal motor neurons, motor

root or peripheral nerve)

Loss of strength

Muscle wasting

Reduced tone

Reduced or absent reflexes

Fasciculations

Cerebellar disorders

History

o Clumsiness, problems with coordination (signs occur on same side as

lesion in brain because fibres cross twice in brainstem)

Examination

o Nystagmus

o Jerky, explosive & loud speech, with irregular separation of syllables

o Arm drift due to hypotonia of agonist muscles

o Hypotonia

o Abnormal finger-nose, rapidly alternating movements & rebound tests

o Abnormal gait

Types

o Midline lesion: truncal ataxia, abnormal hell-toe walk, abnormal

speech

o Bilaternal disease: Hypotonia, abnormal gait, nystagmus

Mini-Mental State Examination

Instructions

Orientation

1. Ask the date. Then ask specifically for parts omitted, for example, 'Can you also

tell me what season it is?' Score 1 point for each correct. 2. Ask in turn, 'Can you tell

me the name of this place?' (town, country, etc). Score 1 point for each correct.

Registration

Ask the patient if you may test his or her memory. Then say the names of three

unrelated objects, clearly and slowly, about one second for each. After you have said

all three, ask him or her to repeat them. This first repetition determines the score (0-

3) but keep saying them until he or she can repeat all three, up to six trials. If he or

she does not eventually learn all three, recall cannot be meaningfully tested.

Attention and calculation

Ask the patient to begin with 100 and count backwards by 7. Stop after five

subtractions (93, 86, 79, 72, 65). Score the total number of correct answers. If the

patient cannot or will not perform this task, ask him or her to spell the word 'world'

backwards. The score is the number of letters in correct order, eg dlrow 5, dlowr 3.

Recall

Ask the patient if he or she can recall the three words you previously asked him or

her to remember. Score 0-3.

Language

Naming: Show the patient a wrist-watch and ask him or her what it is. Repeat for

pencil. Score 0-2.

Repetition: Ask the patient to repeat the sentence after you. Allow only one trial.

Score 0 or 1.

Three-stage command: Give the patient a piece of plain blank paper and repeat the

command. Score 1 point for each part correctly executed.

Reading: On a blank piece of paper, print the sentence 'Close your eyes' in letters

large enough for the patient to see clearly. Ask him or her to read it and do what it

says. Score 1 point only if he or she actually closes his eyes.

Writing: Give the patient a blank piece of paper and ask him or her to write a

sentence for you. Do not dictate a sentence, it is to be written spontaneously. It must

contain a subject and verb and be sensible. Correct grammar and punctuation are

not necessary.

Copying: On a clean piece of paper, draw intersecting pentagons (as below), each

side about one inch and ask him or her to copy it exactly as it is. All ten angles must

be present and two must intersect to score 1 point. Tremor and rotation are ignored.

A score of 20 or less generally suggests dementia but may also be found in acute

confusion, schizophrenia or severe depression. A score of less than 24 may indicate

dementia in some patients who are well educated and who do not have any of the

above conditions. Serial testing may be of value to demonstrate a decline in cognitive

function in borderline cases.

Cerebrovascular Accident

Definition

Stroke. To the public, stroke means weakness, either permanent or transient

on one side, often with loss of speech. Stroke is defined as the clinical

syndrome of rapid onset of cerebral deficit (usually focal) lasting more than 24

hours or leading to death, with no apparent cause other than a vascular one.

Hemiplegia following middle cerebral arterial thromboembolism is the typical

example.

Completed stroke means the deficit has become maximal, usually within 6

hours.

Stroke-in-evolution describes progression during the first 24 hours.

Minor stroke. Patients recover without significant deficit, usually within a

week.

Transient ischaemic attack (TIA). This means a focal deficit, such as a

weak limb, aphasia or loss of vision lasting from a few seconds to 24 hours.

There is complete recovery. The attack is usually sudden. TIAs have a

tendency to recur, and may herald thromboembolic stroke.

CVA is defined as:

- The sudden onset of a focal neurological deficit resulting from either

infarction or hemorrhage within the brain

- Adults 45 years old most likely to have a cardiac source of embolism

- System(s) Affected: Cardiovascular; Nervous

- Synonym(s): Cerebrovascular accident; Reversible ischemic neurological

accident

ALERT

Geriatric Considerations

Amyloid (congophilic) angiopathy is most prevalent in the elderly, especially if the patient also

has dementia.

Pediatric Considerations

Cardiac (especially developmental abnormalities)

Metabolic: Homocystinuria, Fabry disease

Pregnancy Considerations

Parturition may increase the risk of rupture for aneurysm; amniotic fluid embolism may cause

stroke at the time of delivery.

Postpartum period is associated with an increased risk for cerebral venous thrombosis.

General prevention

Stop smoking.

Control blood pressure, diabetes, hyperlipidemia

Use alcohol in moderation, if at all.

Regular exercise

Maintain positive psychological outlook.

Maintain weight control.

Antiplatelet drugs

Angiotensin-converting enzyme inhibitors

Statins

Treat homocystinemia with vitamin B6, vitamin B12, and folic acid.

Anticoagulation when cardioembolism is the suspected cause

Epidemiology

Prevalence

Predominant age: Risk increases over age 45 and is highest in the seventh and

eighth decades

Predominant sex: Male > Female (3:1), but equalises after menopause.

Risk factors

- Age

- Hypertension

- Cardiac disease

- Smoking

- Diabetes

- Antiphospholipid antibodies

- Family history

- Atrial fibrillation

- Hyperlipidemia

- Homocystinemia

Genetics

Inheritance is polygenic with a tendency to clustering of risk factors within families.

Aetiology

Ischemic: Carotid atherosclerotic disease with artery-to-artery thromboembolism

Cardiac:

  -Cardioembolism secondary to valvular (mitral valve) pathology

  -Mural hypokinesias or akinesias with thrombosis (acute anterior myocardial

infarctions or congestive cardiomyopathies)

  -Cardiac arrhythmia (atrial fibrillation)

Hypercoagulable states:

  -Antiphospholipid antibodies, factor V Leiden deficiency, deficiency of protein S,

proteinC

  -Presence of antithrombin 3, oral contraceptives

Other causes:

  -Spontaneous and post-traumatic (i.e., chiropractic manipulation) artery dissection

  -Fibromuscular dysplasia

  -Vasculitis

  -Drugs (cocaine, amphetamines)

Hemorrhagic

Hypertension: May cause damage to putamen, internal capsule, cerebellum,

brainstem, corona radiata

Amyloid (congophilic) angiopathy: Lobar (cortical) hemorrhages in the elderly

Vascular malformations: Arteriovenous malformation, cavernous angioma, venous

angioma, and capillary angioma

Associated Conditions

The major cause of death in the first 5 years after a stroke is cardiac disease.

Diagnosis

Signs and Symptoms

 Carotid circulation (hemispheric): Hemiplegia, hemianesthesia, neglect, aphasia,

visual field defects; less often headaches, seizures, amnesia, confusion

 Vertebrobasilar (brainstem or cerebellar): Diplopia, vertigo, ataxia, facial paresis,

Horner syndrome, dysphagia, dysarthria

 Impaired level of consciousness

 Cerebellar lesion in patients with headache, nausea, vomiting, and ataxia

Tests

Special tests:

 Duplex carotid ultrasonography

 Cerebral angiography

 ECG

 Transthoracic echocardiogram; if normal and a cardiac source is suspected, follow

up with transesophageal echocardiogram

 Holter monitoring

 EEG for suspected seizure

 Prothrombin time (PT) and partial thromboplastin time (PTT); Coumadin prolongs

PT.

 Antiphospholipid antibodies

 Cardiac enzymes

Imaging

Acute phase:

 CT of head

 MRI scan of brain with diffusion-weighted imaging, magnetic resonance

angiography of brain and neck vessels

DDx:

 Migraine

 Focal seizure

 Tumor

 Subdural hematoma

 Hypoglycemia, hyperglycemia, hypercalcemia

Treatment

 Acute phase: Inpatient care, preferably in a stroke unit

 Surgical therapy:

  -In medically fit patients with nondisabling stroke, carotid endarterectomy is

indicated for stenosis of >70% on side ipsilateral to stroke.

  -Medical therapy for 50% stenosis, 50-69% depends on risk factors

General Measures

 Maintain oxygenation.

 Monitor cardiac rhythm for 48 hours.

 Control hyperglycemia (keep glucose 220 mg/dL [12.1 mmol/L]).

 Treat blood pressure >185/110 if patient will be or has been treated with IV tissue

plasminogen activator.

 Do not treat elevated blood pressure unless acute end-organ dysfunction

(encephalopathy, myocardial ischemia, aortic dissection, acute renal failure).

 Prevent hyperthermia

 Early introduction of physiotherapy and ambulation

 Heparin 5,000 units SC q12h

Diet

 Alert with no dysphagia: Diet as tolerated (no added salt if hypertensive)

 Alert with dysphagia: Pureed dysphagia diet or nasogastric feeding tube if

indicated

Activity

Ambulate as soon as possible.

Medication

First Line

 IV tissue plasminogen activator 0.9 mg/kg in highly selected cases within 3 hours

of ischemic stroke

 Enteric-coated aspirin 50-325 mg per day or Dipyridamole-aspirin (Aggrenox):

extended release

 Clopidogrel (Plavix):

 Warfarin

Follow Up

Prognosis

 Variable depending on severity of stroke

 Posterior circulation strokes have a higher acute mortality rate, but generally make

a better functional recovery than hemispheric strokes.

Complications

 Shoulder subluxation

 Hyperextension knee injury

 Depression

 Sympathetic dystrophy

Patient Monitoring

Follow the patient every 3 months for the first year, then yearly.

Parkinson Disease

Definition

An adult-onset neurodegenerative disorder of the extrapyramidal system

characterized by a combination of tremor at rest, rigidity, and bradykinesia

- Diagnosis requires therapeutic response to levodopa, which implies normal striatal

neurons

- Only neurodegenerative disease treatable long term

- System(s) Affected: Musculoskeletal; Nervous

- Synonym(s): Paralysis agitans; Shaking palsy

Epidemiology

Predominant age: 60 years, with 5% between the ages of 21-39

Predominant sex: Male > Female (1.4:1)

Prevalence

In ages 55-64, 0.3%

In ages 65-74, 1%

In ages 75-84, 3.1%

In ages 85-94, 4.3%

ALERT

Geriatric Considerations

Common among elderly

Paediatric Considerations

May occur as secondary parkinsonism in this age group

Risk Factors

Unknown in the idiopathic disease

Association between smoking and increased caffeine intake and reduced risk for

Parkinson disease has been reported.

Genetics

May be a genetic role, with risk 2.95-fold in patients with positive family history in

late-onset disease, 7.76-fold increase in early-onset disease (age 50 years)

Aetiology

 Unknown

 Loss of dopaminergic neurons in the substantia nigra, with rate of loss 1% per year

in patients with Parkinson vs. 0.5% in normal aging

 No clear environmental causes identified

 Known toxins: MPTP, pesticides. Other nondopaminergic neurons may be

affected.

Associated Conditions

 Psychosis

 Depression

Diagnosis

Signs and Symptoms

 Cardinal signs:

  -Tremor (4-8 Hz) in repose: Diagnostic, but not required; relieved with activity,

concentration, and sleep; increases with stress; 10% of patients present with only

tremor, 30% present without; most begin with unilateral tremor

  -Bradykinesia: Required for diagnosis; most disabling symptom; movement initiation

difficult, causes the gait and postural abnormalities; fine, repetitive movements

affected more than large

  -Rigidity: Lead-pipe type; cogwheel with tremor

 Common presentation:

  -Asymmetric tremor

  -Clumsy or weak limb: Early sign of bradykinesia

  -Stiff or uncomfortable limb: Early rigidity

  -Gait disorder: Asymmetric slowness, shuffling, reduced arm movement or

imbalance

 Other associated signs and symptoms:

  -Speech is poorly enunciated, low volume, clipped

  -Ocular abnormalities: Decreased blinking, blepharospasm, impaired upward gaze

  -Seborrhea

  -Dysautonomia with constipation, incontinence, sexual dysfunction

  -Depression in 2/3 of patients

  -Dementia in 20% of patients mild to moderate

  -Gait disturbances including no arm swing, en mass turning, problems getting up

from chair, festination, freezing

  -Leaning posture

  -Propulsion or retropulsion

  -Micrographia

  -Mask faces

  -Neglect of swallowing with drooling

 Hoehn and Yahr scale of disability:

  -Stage 1: Unilateral, minimal functional impairment

  -Stage 2: Bilateral, without impairment of balance

  -Stage 3: Bilateral, positive instability; patient is physically independent

  -Stage 4: Severe disability; patient can walk or stand without assistance, but is

markedly incapacitated

  -Stage 5: Patient is wheelchair bound or bedridden unless aided

Physical Exam

Diagnostic criteria:

 Clinically definite if any 3 of the following are present or any 2 of the 1st 3 display

asymmetry:

  -Rest tremor

  -Rigidity

  -Bradykinesia

  -Impaired postural reflexes

Tests

Imaging

 CT or MRI to help rule out other disorders

 Positron emission tomography scanning

Pathological Findings

Lewy bodies

Ddx:

 Parkinsonism: Bradykinesia with little or no response to levodopa, indicating that

the striatal neurons are also degenerated:

  -Progressive supranuclear palsy

  -Multisystem atrophy

  -Alzheimer with extrapyramidal features

  -Side effects of neuroleptic medications

  -Infectiouspostencephalitic

  -Vascularlacunar state

  -Toxins

  -Metabolic Wilson disease: Onset at age 40

 Benign essential tremor: Positive family history and relief with alcohol

 Consider other conditions if:

  -Falls or early dementia

  -Symmetric Parkinsonism

  -Wide-based gait

  -Abnormal eye movements

  -Orthostatic hypotension

  -Babinski sign

  -Urinary retention

  -Rapid progression

Treatment

General Measures

 Drugs have therapeutic and toxic effects.

 Acute worsening may indicate depression, noncompliance, or supervening illness.

 Course is progressive with or without drugs. Lifelong therapy directed toward

symptom control treat disability

 Investigate for drug-induced cause; if found, discontinue drug. Symptom resolution

may take weeks to months.

Diet

 Small, frequent meals if difficulty in eating

 High liquid intake important; high-bulk foods

 Reduced-protein diet is unnecessary

Activity

Maintain activity at whatever level possible; use cane for walking

Medication

First Line

 Levodopa/carbidopa (Sinemet): Most effective and the initial drug of choice in older

patients with more severe symptoms, speech disorders and falls are resistant to

levodopa:

 Dopamine agonists slightly less effective; long half-life; reduces wearing-off effects

of levodopa. Add when levodopa >500 mg per day. Early monotherapy may reduce

levodopa use and long-term side effects. May be initial drug of choice in younger

patients with milder symptoms. Usually need addition of levodopa in 1st 5 years of

monotherapy. Avoid with dementia

Adjuvant Drugs

 Tricyclic antidepressants for nighttime sedation and associated depression (50% of

patients with Parkinson)

 Apomorphine as agonist or for freezing (use limited by adverse effects [vomiting]

and need for parenteral administration)

 Clozapine: 70-200 mg suppress frequency of dyskinesia and increase "on" time;

also useful for hallucinations (50 mg/day). Side effects include sedation, sialorrhea,

and agranulocytosis.

 Donepezil: 5 mg; cognitive impairment

 Modafinil: 100-200 mg excessive daytime sleepiness

SURGERY

 Adrenal medullary transplants unproven

 Thalamotomy akinesia

 Stereotactic pallidotomy akinesia

 Deep brain stimulation of subthalamic nucleus dyskinesia, tremor response 88%;

may worsen pre-existing psychiatric disorders; fewer "off" problems, fewer "on"

dyskinesias, and 50% reduction of medications

Follow up

Prognosis

 More rapid progression: Older at disease onset; dementia

 Milder disease: Predominant feature is tremor

Ccomplications

 Aspiration pneumonia

 Falls

 Associated with a 2-fold increase in risk of death

Patient Monitoring

Lifelong

Dementia

Definition

A pathologic process defined as a persistent impairment of a prior level of intellectual

functioning

 Alzheimer dementia (AD):

  -Characterized by relentless deterioration of higher cortical functioning

  -Variable rate of deterioration

 Vascular dementia (VaD):

  -Formerly multi-infarct dementia

  -Caused by clinical or subclinical cerebral infarcts secondary to atherosclerosis

  -Stepwise deterioration with periods of clinical plateaus

 Dementia with Lewy bodies (DLB):

  -Early-onset dementia with associated psychosis, depression

 Frontotemporal dementia (FTD):

  -Insidious change in personality with cognitive dysfunction

  -Onset usually prior to age 65

General prevention

Ischemic-vascular dementia: General stroke prevention (lipid, diabetes, blood

pressure control)

Epidemiology

Predominant age: Increasing incidence with increasing age

Predominant sex: Male = Female

Incidence

Between ages 60-64 years: 0.5%

Between ages 80-90 years: 3.2%

1,480/100,000

Risk factors

Increasing age

Prevalence of atherosclerotic disease (VaD)

History of head trauma

History of CNS infection

Midlife depression (VaD)

Genetics

At least 15% of patients with AD will report a positive family history

Persons with Trisomy 21 (Down syndrome) who survive into their 20s and 30s will

inevitably develop a progressive dementia

Aetiology

 AD:

  -Genetic predisposition in more than 15%

 VaD

  -Cerebral atherosclerosis or emboli with clinical or subclinical infarcts

 Secondary dementias: Causes include hypothyroidism, vitamin B deficiency,

normal pressure hydrocephalus, AIDS, syphilis, and various medications.

Diagnosis

Signs and Syptoms

 Impaired short-term and long-term memory

 Impaired abstract thinking

 Impaired judgment

 Aphasia

 Apraxia

 Agnosia

 Anomia

 Personality change, emotional outbursts, wandering, restlessness, hyperactivity,

especially with FTD

 Sleep disturbances

 Mood disturbances

 Urinary incontinence (usually late in AD or normal pressure hydrocephalus)

 Fecal incontinence (late)

 Rigidity

 Tremor (especially with DLB)

 Hallucinations (especially with DLB)

 Delusions

 Overt paranoid behavior

 Weight loss

 Seizures

Tests

 Mental status testing

 Neuropsychologic testing

 Electroencephalogram for patients with altered consciousness or associated

seizures

Lab

Done primarily to rule out potentially reversible causes:

 Thyroid function tests

 Syphilis serology

 Serum B12 and folate levels

 CBC and screening metabolic profile

 Drugs that may alter lab results: Thyroid hormone replacement and iodine

preparations may affect thyroid function tests.

 Disorders that may alter lab results: False positive syphilis serology with acute

infections, leprosy, subacute bacterial endocarditis, and autoimmune disorders

Imaging

 Head CT if history suggestive of a mass, or focal neurologic signs or in patient with

dementia of brief duration

 MRI

  -More sensitive than CT for detection of soft-tissue lesions (small infarcts, mass

lesions, atrophy of the brainstem, and other subcortical structures).

  -May also clarify ambiguous CT findings.

 Isotope cisternography if suspicious of normal pressure hydrocephalus

 Positive emission tomography shows cortical hypometabolism

Pathological Findings

 AD:

  -Diffuse cerebral atrophy in association areas, hippocampus, amygdala

  -Granulovesicular degeneration

  -Neurofibrillary tangles

  -Senile neuritic plaques

  -Microvascular amyloid

 VaD:

  -Old infarcts, lacunes

  -Manifestations of atherosclerotic disease

Ddx:

 Delirium

 Normal aging

 Mild cognitive impairment

 Depression

 Schizophrenia

 Chronic alcoholism

 Postsurgical and/or postanesthesia state

 Normal Pressure Hydrocepahalus

Treatment

General Measures

 Daily schedules and written directions

 Support and education of caregivers

 Emphasis on nutrition, personal hygiene, personal safety (accident-proofing the

home), and supervision

 Discussions with the family concerning advance directives

 Socialization (adult day care)

 Sensory stimulation (prominent displays of clocks and calendars)

 Improvement in sleep hygiene

 Pharmacotherapy should be reserved for specific behavioral symptoms after non-

pharmacologic therapy has failed

Diet

No special diet

Activity

Fully active with direction and supervision

Medications

 Aggressive behaviors: Antipsychotics such as risperidone (Risperdal) 0.5-1.0 mg,

olanzapine (Zyprexa) 2.5 mg, or quetiapine (Seroquel) 25 mg PO at bedtime are

reasonable choices in a non-emergency situation (3)[B]. Other options include

carbamazepine (Tegretol) 100 mg b.i.d.-t.i.d. or Valprioc acid 250-1,500 mg daily in

divided dose

 Depression: Use serotonin reuptake inhibitors: Sertraline (Zoloft), fluoxetine

(Prozac), paroxetine (Paxil), citalopram (Celexa), or escitalopram (Lexapro) all orally.

Start with half the usual starting dose.

 Sleep disturbance: Intermittent use of temazepam (Restoril) 7.5-15 mg, zolpidem

(Ambien) 5 mg, trazodone (Desyrel) 25-50 mg, or mirtazapine (Remeron) 7.5 mg at

bedtime is occasionally warranted

 Cognitive dysfunction: Donepezil (Aricept) 5-10 mg daily, rivastigmine (Exelon)

1.5-6 mg b.i.d., galantamine (Reminyl) 4-12 mg (4)[B], memantine (Namenda) 5-20

mg daily PO

Prognosis

 AD: A progressive disease with variable rates of progression, but inevitably leading

to profound cognitive impairment

 VaD: Less likely to be progressive, but cognitive improvement is unlikely

 Secondary dementias: Treatment of the underlying condition may lead to

improvement

Patient Monitoring

 Periodic mental status testing to assess progression and predict prognosis

 Periodic monitoring of nutritional status

 Periodic monitoring of the caregiver status to assess for caregiver stress

 Periodic assessment of the environment for safety

Cerebella Disorders

The third system of motor control modulates coordination, rather than speed. Ataxia,

i.e. unsteadiness, is characteristic when it malfunctions.

The cerebellum receives afferent fibres from:

proprioceptive receptors in joints and muscles

vestibular nuclei

basal ganglia

the corticospinal system

olivary nuclei.

Efferent fibres pass from the cerebellum to:

each red nucleus

vestibular nuclei

basal ganglia

corticospinal system.

Each lateral cerebellar lobe coordinates movement of the ipsilateral limbs. The

vermis (a midline structure) is concerned with maintenance of axial (midline) posture

and balance.

Cerebellar lesions

Expanding mass lesions within the cerebellum obstruct the aqueduct to cause

hydrocephalus, with severe pressure headaches, vomiting and papilloedema. Coning

of the cerebellar tonsils through the foramen magnum and respiratory arrest occur,

often within hours. Rarely, tonic seizures (sudden attacks of limb stiffness) occur.

Lateral cerebellar lobes

A lesion within one cerebellar lobe (e.g. a tumour or infarction) causes disruption of

the normal sequence of movements (dyssynergia) on the same side. Ataxia and

other signs develop.

A lesion within one cerebellar lobe (e.g. a tumour or infarction) causes disruption of

the normal sequence of movements (dyssynergia) on the same side. Ataxia and

other signs develop. Neurotransmitter changes in cerebellar disease are poorly

understood.

Posture and gait

The outstretched arm is held still in the early stages of a cerebellar lesion (cf. the drift

of a pyramidal lesion) but there is rebound upward overshoot when the limb is

pressed downwards and released. Gait becomes broad and ataxic; the patient falters

towards the lesion.

Tremor and ataxia

Movement is imprecise in direction, in force and in distance (dysmetria). Rapid

alternating movements (tapping, clapping or rotary hand movements) are clumsy and

disorganized (dysdiadochokinesis). Intention tremor (action tremor, with past-

pointing) is seen. Speed of movement is preserved, cf. extrapyramidal disease.

Nystagmus

Coarse horizontal nystagmus develops with lateral cerebellar lobe lesions - the fast

component towards the lesion.

Dysarthria

A halting, jerking dysarthria occurs - the scanning speech of cerebellar lesions

(usually bilateral).

Other signs

Principal causes of cerebellar syndromes

Tumours Haemangioblastoma

  Medulloblastoma

  Secondary neoplasm

  Compression by acoustic neuroma

Vascular lesions Haemorrhage

  Infarction

  Arteriovenous malformation

Infection Abscess

  HIV

  Kuru

Developmental Arnold-Chiari malformation

  Basilar invagination

  Cerebral palsy

Toxic and metabolic Anticonvulsant drugs

  Chronic alcohol abuse

  Following carbon monoxide poisoning

  Lead poisoning

  Solvent abuse

Inherited Friedreich's ataxia

  Ataxia telangiectasia

  Essential tremor

Miscellaneous Multiple sclerosis

  Hydrocephalus

  Postinfective cerebellar syndrome of childhood

  Hypothyroidism

  Non-metastatic manifestation of malignancy

  Cerebral oedema of chronic hypoxia

Titubation - rhythmic head tremor in either to and fro ('yes-yes') movements or rotary

('no-no') movements - also occurs, mainly when cerebellar connections are involved

(e.g. in essential tremor and MS). Hypotonia (floppy limbs) and depression of

reflexes (and slow, pendular reflexes) are also sometimes seen with cerebellar

disease, though of little value as localizing signs.

Midline cerebellar lesions

Midline cerebellar vermis lesions have a dramatic effect on trunk and axial

musculature-difficulty standing and sitting unsupported, with a rolling, broad, ataxic

gait (truncal ataxia). Lesions of the flocculonodular region of the cerebellum cause

vertigo, vomiting and gait ataxia if they extend to the roof of the fourth ventricle.

Tremor

Tremor means a regular and sinusoidal oscillation. Different varieties are outlined

below. Pathological anatomy and neurotransmitter changes remain largely unknown.

Postural tremor

Everyone has a physiological tremor (often barely perceptible) of the outstretched

hands at 8-12 Hz. This is increased with anxiety, caffeine, hyperthyroidism and

certain drugs (sympathomimetics, sodium valproate, lithium) or in mercury poisoning.

A coarser, postural tremor is seen in benign essential tremor (usually at 5-8 Hz) and

in chronic alcohol abuse. Postural tremor does not worsen on movement, though it

may become more obvious.

Intention tremor

Tremor exacerbated by action, with past-pointing and accompanying incoordination

of rapid alternating movement (dysdiadochokinesis), occurs in cerebellar lobe

disease and with lesions of cerebellar connections. Titubation and nystagmus may

be present.

Rest tremor

This tremor occurs typically in Parkinson's disease, and is noticeably worst at rest,

usually between 4 and 7 Hz - 'pill-rolling' between thumb and index finger.

Other tremors

Coarse tremor is seen following lesions of the red nucleus (e.g. infarction,

demyelination) and rarely with frontal lobe lesions.

Peripheral Nerve Disease

The various nerve fibre types are shown in the table below. All are myelinated except

C fibres that carry impulses from pain receptors.

A, B and C fibres in peripheral nerves

Diameter

(μ) Conduction velocity m/s Function

Aα(1-20) 70-110 Motor; proprioception

Aβ(5-10) 30-60 Touch

Aγ(3-6) 20-30 Fusimotor, to spindles

Aδ(2-5) 20-30 Sharp pain

B (< 3) 5-15 Autonomic, preganglionic

C (< 1.3) 0.5-2 Slow pain

Mechanisms of damage to peripheral nerves

Peripheral nerves consist of two principal cellular structures - the axon and its

anterior horn cell, and the myelin sheath, produced by Schwann cells between each

node of Ranvier. Blood supply is via vasa nervorum. Six principal mechanisms, some

coexisting, cause nerve malfunction.

1. Demyelination

When the Schwann cell is damaged, the myelin sheath is disrupted. This causes

marked slowing of conduction, seen for example in Guillain-Barré syndrome, post-

diphtheritic neuropathy and many hereditary sensorimotor neuropathies.

2. Axonal degeneration

The primary damage is in the axon, which dies back from the periphery. Conduction

velocity tends to remain normal because axonal continuity is maintained in surviving

fibres. Axonal degeneration occurs typically in toxic neuropathies.

3. Wallerian degeneration

This describes the changes following nerve section. Both axon and distal myelin

sheath degenerate over several weeks.

4. Compression

Focal demyelination at the point of compression. The myelin sheath is disrupted. This

occurs typically in entrapment neuropathies e.g. carpal tunnel syndrome.

5. Infarction

Microinfarction of vasa nervorum occurs in arteritis, e.g. polyarteritis nodosa, Churg-

Strauss syndrome, and in diabetes mellitus. Wallerian degeneration occurs distal to

the ischaemic zone.

Nerve regeneration

Regeneration occurs either by remyelination, when recovering Schwann cells spin

new myelin sheaths around the axon, or by axonal growth down the nerve sheath

and sprouting from the axonal stump. Axonal growth takes place at a rate of up to 1

mm daily.

Defeintion:

Peripheral neuropathies - The type of neuropathy (axonal or demyelinating)

can be assessed by electrical nerve studies. Neuropathy means a

pathological process affecting a peripheral nerve or nerves.

Mononeuropathy means a process affecting a single nerve.

Mononeuritis multiplex (multiple mononeuropathy, or multifocal neuropathy)

affects several or multiple nerves.

Polyneuropathy describes diffuse, symmetrical disease, usually beginning

peripherally. The course is either acute, chronic, static, progressive, relapsing

or towards recovery. Polyneuropathies are motor, sensory, sensorimotor (i.e.

mixed) and autonomic. They are classified broadly into demyelinating and

axonal types, depending upon which principal pathological process

predominates. It is often impossible to separate these clinically. Many

different classifications exist. Many systemic diseases cause neuropathies.

Widespread loss of tendon reflexes is typical.

Radiculopathy means disease affecting nerve roots.

Diagnosis is made by clinical pattern, electrical tests, nerve biopsy (usually sural or

radial) and identification of systemic or genetic disease.

Delirium

Definition

· A neurologic complication of illness and/or medication(s) especially common in

older patients

· A medical emergency requiring immediate evaluation to decrease morbidity and

mortality

· System(s) Affected: Nervous

· Synonym(s): Acute confusional state; Altered mental status; Organic brain

syndrome; Acute mental status change

Epidemiology

· Predominant age: Older persons

· Predominant sex: Male = Female

Incidence

· 25-60%

· >50% in high-risk older patients

Prevalence

10-40% in hospitalised older patients

Risk Factors

Predisposing risk factors:

· Advanced age

· Prior cognitive impairment

· Functional impairment

· High blood urea nitrogen (BUN): Creatinine ratio

· Dehydration

· Malnutrition

· Hearing or vision impairment

· Frailty Precipitating risk factors:

· Severe illness in any organ system(s)

· Need for a urinary catheter

· >3 medications

· Pain

· Any adverse iatrogenic event

· Medications, especially long-acting sedative hypnotics (e.g., diazepam and

flurazepam), narcotics (especially meperidine), and anticholinergics (especially

diphenhydramine)

Pathophysiology

· Neuropathophysiology is not clearly defined

· Multicomponent approach addressing contributing factors can reduce incidence and

complications

Aetiology

Usually multifactorial:

· Often interaction between predisposing and precipitating risk factors

· With more predisposing factors (i.e., the frailer the patients), fewer precipitating

factors needed to produce delirium

· If few predisposing factors (e.g., very robust patients) more precipitating factors

needed to manifest delirium

Associated Conditions

Multiple, but most common are

· New medicine or medicine changes

· Infections (especially lung and urine, but meningitis needs consideration as welll)

· Toxic-metabolic (Especially low sodium, elevated calcium, renal failure and hepatic

failure)

· Heart attack

· Stroke

· Alcohol or drug withdrawal

Diagnosis

Pre-Hospital

The Confusion Assessment Method (CAM - Mini Mental) may be applied either pre-

hospital or in hospital, and has been adapted for the ICU setting (CAM-ICU)

ALERT

· Key diagnostic features comprise the CAM.

  -Acute change in mental status that fluctuates

  -Abnormal attention

  -and either disorganized thinking or altered level of consciousness

· Any of the following non-diagnostic symptoms may be present:

  -Short- and long-term memory problems

  -Sleep-wake cycle disturbances

  -Hallucinations and/or delusions

  -Emotional lability

  -Tremors and asterixis

· Subtypes based on level of consciousness:

  -Hyperactive delirium (15%): Patients are loud, rambunctious, and disruptive.

  -Hypoactive delirium (20%): Quietly confused; may sit and not eat, drink, or

move

  -Mixed delirium (50%): Features of both hyperactive and hypoactive delirium

  -Normal consciousness delirium (15%): Still display disorganized thinking, along

with acute onset, inattention, and fluctuation.

History

· Time course of mental status changes

· Recent medication changes

· Symptoms of infection

· New neurologic signs

Physical Exam

· Good cardiorespiratory exam essential

· Focal neurologic signs usually absent

· Mini-mental state exam helpful as structured interview and to follw course over time

Tests

ECG as necessary

Lab

· CBC

· Electrolytes, BUN, and creatinine

· Urinalysis, urine culture

· If needed:

  -Arterial blood gases

  -Drug screen

  -Liver function tests

Imaging

· Chest radiograph

· Non-contrast-enhanced head (CT) scan if:

  -Unclear diagnosis

  -Recent fall

  -Receiving anticoagulants

  -New focal neurologic signs

  -To rule out increased intracranial pressure before lumbar puncture

Diagnostic Procedures/Surgery

Lumbar puncture:

· Rarely necessary

· Perform if clinical suspicion of a CNS bleed or infection is high.

DDx:

· Depression (slow onset, disturbance of mood, normal level of consciousness, and

fluctuates over weeks to months)

· Dementia (insidious onset, memory problems, normal level of consciousness, and

fluctuates over days to weeks)

· Psychosis (rarely sudden onset in older adults)

Treatment

Pre-Hospital

· Stabilise vitals if needed.

· Ensure immediate evaluation.

General measures

· Postoperative patients should be monitored and treated for the following:

  -Myocardial infarction/ischemia

  -Pulmonary complications/pneumonia

  -Pulmonary embolism

  -Urinary or stool retention (attempt catheter removal by postoperative day 2)

· Anesthesia route (general epidural) does not affect the risk of delirium

· Multifactorial treatment: Identify contributing factors and provide pre-emptive care to

avoid iatrogenic problems (2-4)[A] with special attention to:

· Central nervous system oxygen delivery (attempt to attain the following):

  -SaO2 >90% with goal of SaO2 >95%

  -Systolic blood pressure <2/3 of baseline or >90 mm Hg

  -Hematocrit >30%

· Fluid/electrolyte balance:

  -Sodium, potassium, and glucose normal (glucose <300 mg/dL in diabetics)

  -Treat fluid overload or dehydration

· Treat pain:

  -Schedule acetaminophen (1 g q.i.d.) if daily pain

  -Morphine or oxycodone for breakthrough pain if acetaminophen ineffective

ALERT

Avoid meperidine (Demerol)

· Eliminate unnecessary medications:

  -Investigate new symptoms as potential medication side effects

· Regulate bowel/bladder function:

  -Bowel movement at least every 48 hours

  -Screen for urinary retention or incontinence, especially after catheter removal

· Prevent major hospital-acquired problems:

  -6-inch-thick foam mattress overlay or a pressure-reducing mattress

  -Avoid urinary catheter

  -Incentive spirometry, if bed bound

  -Subcutaneous heparin 5,000 u b.i.d., if bedfast

· Environmental stimulation:

  -Glasses and hearing aids

  -Clock and calendar

  -Soft lighting

  -Radio, tapes, and television, if desired

· Sleep:

  -Quiet environment

  -Soft music

  -Therapeutic massage

· Restraints do not reduce risk of falls/injury:

  -Use only in the most difficult-to-manage patients, as briefly as possible

Diet

· Dentures used properly

· Proper positioning for meals

· Assistance with meals when necessary

· Nutritional supplements (1-3 cans daily) if intake is poor

· Temporary nasogastric tube if unable to eat and bowels working

Activity

· As tolerated

· Early physical therapy consultation to prevent deconditioning

Nursing

· IInstitute skin care program for patients with established incontinence

· Turning regimen if at risk of pressure ulcers

Special Therapy

Physical Therapy

Early mobilization critical:

· Out of bed on hospital day 2 (or postoperative day 1) if no contraindications

· Out of bed several hours daily if able

· Daily therapy if not ambulating independently

· Daily therapy if not functionally independent

IV Fluids

As needed for dehydration

Medication

· Nonpharmacologic approaches are preferred for initial treatment

· Medications often treat only the symptoms and do not address the underlying cause

First Line

· Neuroleptics:

  -Haloperidol (Haldol): initially, 0.25-0.5 mg PO/IM/IV unless urgent sedation needed

  -Quetiapine (Seroquel): 25 mg daily to b.i.d.

· Short-acting benzodiazepines, if neuroleptics do not work or should be avoided:

  -Lorazepam (Ativan): initially, 0.25-0.5 mg PO/IM/IV q6-8h, may need to adjust to

effect (caution in patients with impaired liver function).

· Risperidone (Risperdal): 0.25-0.5 mg PO daily

· Contraindications: Avoid neuroleptics in patients with parkinsonism or Parkinson

disease.

· Precautions: Neuroleptics may cause extrapyramidal effects, and benzodiazepines

may lead to sedation. Both increase the risk of falls.

Follow up

Admission Criteria

New delirium is a medical emergency and requires admission except in the setting of

palliative home care

Discharge Criteria

· Resolution of precipitating factor(s)

· Safe discharge site if still delirious

Issues for Referral

· If delirium at discharge, will usually be followed in post-acute facility

· If no delirium at discharge, follow-up with primary care physician in 1-2 weeks

Prognosis

Usually improves with treatment of underlying condition, but may become chronic.

Ccomplications

· Falls

· Pressure ulcers

· Malnutrition

· Functional decline

· Versedation

· Polypharmacy

Patient Monitoring

· Evaluate and assess mental status daily.

· Other depends on specific conditions present.

Falls

Falls are a major problem for elderly people, especially women. Some 30% of

community-dwelling elderly individuals fall each year, and the proportion increases

with age. Nonetheless, falling must not be viewed as accidental, inevitable, or

untreatable.

Epidemiology:

Falls are the most common cause of injury in patients over 65 years of age. Fifty

percent of elderly persons who fall do so repeatedly.

Aeitology:

Balance and ambulation require a complex interplay of cognitive, sensory,

neuromuscular, and cardiovascular function and the ability to adapt rapidly to an

environmental challenge. With age, balance becomes impaired and sway increases.

The resulting vulnerability predisposes the older person to fall when challenged by an

additional insult to any of these systems. Thus, a seemingly minor fall may be due to

a serious problem, such as pneumonia or a myocardial infarction.

Much more commonly, however, falls are due to the complex interaction between a

variably impaired patient and an environmental challenge. While a warped floorboard

may pose little problem for a vigorous, unmedicated, alert person, it may be sufficient

to precipitate a fall and hip fracture in the patient with impaired vision, strength,

balance, or cognition. Thus, falls in older people are rarely due to a single cause, and

effective prevention entails a comprehensive assessment of the patient's intrinsic

deficits (usually diseases and medications), the routine activities, and the

environmental obstacles.

Intrinsic deficits are those that impair sensory input, judgment, blood pressure

regulation, reaction time, and balance and gait. Medications and alcohol use are

among the most common, significant, and reversible causes of falling. Other

treatable contributors include postprandial hypotension (which peaks 30 to 60 min

after a meal), insomnia, urinary urgency, foot problems, and peripheral edema [which

can burden impaired leg strength and gait with an additional 2 to 5 kg (5 to 10 lb)].

Since most falls occur in or around the home, a visit by a visiting nurse, physical

therapist, or physician often reaps substantial dividends.

Falls

Most individuals who fall will do so on a level surface and most will suffer an isolated

orthopedic injury. Falls are reported as the underlying cause of 9500 deaths each

year in patients older than age of 65 years. Many falls in the elderly population occur

in residential institutions such as nursing homes. In the >85-year-old age group, 20

percent of fatal falls occur in nursing homes.

There are age-related changes in postural stability, balance, motor strength,

coordination, and reaction time that make the elderly more prone to tripping and

falling, and may explain the increased incidence of falls. Also, decreased visual

acuity and increased memory loss can cause the patient difficulty in recognizing and

avoiding environmental hazards. Acute, preexisting, and chronic diseases also may

lead to falls. Syncope has been implicated in many cases of elderly patients who fall

and this may be secondary to dysrhythmias, venous pooling, autonomic

derangement, hypoxia, anemia, or hypoglycemia. Other contributing factors include

alcohol and medications, most notably sedative, antihypertensive, antidepressant,

diuretic, and hypoglycemic agents.

Falls are not a normal part of aging. A fall is a symptom, and emergency physicians

need to assess both the cause and the consequences of the fall. The causes of a fall

may include acute or chronic diseases, medications, and environmental factors.

Consequences of a fall include injury and fear of falling, resulting in a decrease in

activities. A fall can represent a sentinel event in an older person's life and result in a

downward spiral of decreased activities, leading to death.

As many as 50 percent of older patients admitted to the hospital after a fall die within

1 year. An emergency physician should obtain the history of what caused the fall and

determine whether further ED screening tests (electrocardiography, computed

tomography, laboratory tests, social service consultation, etc.) need to be done to

evaluate the cause. The patient should then be informed about fall assessment

programs that decrease the incidence and morbidity from falls.

Complications of Falls and Treatment

One out of four people who fall suffers serious injury. About 5% of falls result in

fractures, and an equal proportion cause serious soft tissue damage. Falls are the

sixth leading cause of death for older people and a contributing factor in 40% of

admissions to nursing homes. Resultant hip problems and fear of falls are major

causes of loss of independence.

Subdural hematoma is a treatable but easily overlooked complication of falls that

must be considered in any elderly patient presenting with new neurologic signs,

including confusion alone, even in the absence of a headache. Dehydration,

electrolyte imbalance, pressure sores, rhabdomyolysis, and hypothermia may also

occur and endanger the patient's life following a fall.

The risk of falling is related to the number of contributory conditions. Because the

relationship is multiplicative rather than additive, however, even minor improvement

in a number of these factors will reduce