Neurology Cases

8/8/2019 Neurology Cases

1/16

Neurology

cases


2/16


3/16

NEUROLOGY CASES

31

Diagnosis: Stroke affecting the right side

GENERAL APPEARANCE: May have contractures on affected side, may have

obvious facial droopTONE: Usually increased

(unless acute) on

affected side

POWER: Reduced on affected

side

REFLEXES: Hyper-reflexia on

affected side

SENSATION: Usually intact, but

may have sensoryinattention

COORDINATION: Normal (but may be

impossible to assess

due to decreased

power)

OTHER: Patient may have

dysphasia and

homonymous hemianopiaCAUSES: Infarct or haemorrhage

MARKERS OF SEVERITY: Inattention, absent power, contractures

NOTES: Strokes affecting the right side are caused by left

sided cerebral lesions. As a consequence, Brocas

and/or Wernickes areas may be affected. This

may result in an expressive and/or receptive

dysphasia. Reception can be tested by one, two

and three stage commands. The patient may have a

homonymous hemianopia on the same side as theclinical findings.

H E L !

troke is the commonest neuro-

ogy case in finals, so knowing it

ell is important. Common ques-

ions are: what types of strokes

re there? how do you clinically

istinguish between infarct and

aemorrhage (headache, loss

of consciousness, coma)? whats the treatment for an infarct

aspirin, risk factor management,

ultidisciplinary care, carotid

oppler if good recovery)?

Practise talking about the site

f a lesion and causes and sites

f visual defects.


4/16

4 WEEKS TO FINALS

32

Diagnosis: Stroke affecting the left side

GENERAL APPEARANCE: May have contractures on affected side. May have

facial droopTONE: Increased on affected

side

POWER: Decreased on affected

side

REFLEXES: Hyper-reflexia on

affected side

SENSATION: Usually normal (but

check for inattention)

COORDINATION: Normal (but may behard to assess)

OTHER: Look for contractures

and homonymous

hemianopia

CAUSES: Infarct or

haemorrhage

MARKERS OF SEVERITY: Contractures,

inattention,immobility

NOTES: Left sided strokes are

usually caused by a lesion in the right hemisphere.

As a consequence Brocas area and Wernickes

area are preserved. Lesions of the right hemisphere

can cause apraxia or neglect. A lesion in the

right hemisphere can cause a left homonymous

hemianopia.

H EL P !

The commonest questions for

stroke are detailed on the previ-

us page. It is essential to know

bout the multidisciplinary

are of stroke. Early physio-

therapy for early mobilisation

nd prevention of contractures..

T assessment to ascertainevel of independence and to

ttempt discharge home with

the necessary aids. Appropriate

ursing care on a dedicated

stroke ward is also part of the

ational guidelines. Speech

herapy including swallowing

ssessment and assistance

ith speech deficits is also

ssential.


5/16

NEUROLOGY CASES

33

Diagnosis: Cerebellar Signs

GENERAL APPEARANCE: May be in wheelchair if patient has multiple

sclerosis (MS)TONE: Reduced on affected

side (although some

cerebellar syndromes

may be bilateral)

POWER: Normal

REFLEXES: Normal

SENSATION: Normal

COORDINATION: Impaired with

past pointing andintention tremor

OTHER: Nystagmus,

dysdiadochokinesia,

ataxia, slurred

speech

CAUSES: Commonest

causes are stroke,

MS, alcohol,anticonvulsant

therapy and paraneoplastic syndromes (lung

cancer)

NOTES: The commonest cause ofbilateralcerebellar signs

is MS. Check for an internuclear ophthalmoplegia

when you look for nystagmus. If the diagnosis is

MS, ophthalmoscopy may reveal optic disc pallor.

Is the patient in a wheelchair? Are they relatively

young? All these will point to MS. Strokes willtend to cause a unilateralcerebellar syndrome.

H E L !

emember DANISHsdiadochokinesia

taxia

ystagmus

tention tremor

urred speech

potonia

These are the main signs in a

erebellar syndrome. Make sure

ou know the more common

auses as this is the most com-

on question to come up.

You may get asked to assess

he speech. Ask the patient to

ay British Constitution or bib

al riticism.


6/16

4 WEEKS TO FINALS

34

Diagnosis: Parkinsons Disease

GENERAL APPEARANCE: Mask-like face and resting pill-rolling tremor

TONE: Increased, with cog-wheeling or lead-piping ifsevere

POWER: Normal

REFLEXES: Hyper-reflexia

SENSATION: Normal

COORDINATION: Normal

OTHER: Shuffling gait,

difficulty initiating

movement

CAUSES: Parkinsonsdisease is caused

by degeneration

of the cells in the

substantia nigra

and pigmented

neurones. This

leads to a reduced

level of dopamine.Other causes

of a Parkinsonian syndrome are antipsychotic

medications.

NOTES: Parkinsons disease is a syndrome of bradykinesia,

tremor and rigidity. It is commonly unilateral.

Treatment should be withheld for as long as

possible as the medications used either wear off

or can cause unwanted side effects with long-term

use (dyskinesia). Medications available are L-dopawith a dopa-decarboxylase inhibitor, dopa agonists

or COMT antagonists.

H EL

This is very common in finals and

a diagnosis that you should be

ble to make from the end of the

ed.

Common questions relate to

he causes, and the treatment.

Ensure that you test the

patients gait and functions suchas doing up buttons and writing,

as this shows your awareness

of the practical problems that

atients face.

Also try and mention multi-

disciplinary care with OT and

hysiotherapy to maintain

ni dependence for as long as

ossible.


7/16

NEUROLOGY CASES

35

Diagnosis: Old Polio

GENERAL APPEARANCE: Shortened wasted limb

TONE: ReducedPOWER: Reduced/absent

REFLEXES: Absent

SENSATION: Normal

COORDINATION: Normal (if able)

CAUSES: Poliomyelitis

NOTES: Polio affects the

anterior horn cells

and motor neurones

of cranial nerves. Itmay start with a GI

infection. It can then progress to an asymmetrical

paralysis. In children, it will result in failure of

growth of the limb resulting in a shortened wasted

limb with lower motor neurone signs. Treatment is

supportive and patients may require ventilation.

H E L !

olio can be distinguished from

uillainBarr by its asymmet-

ical nature. In an exam, the key

s the shortened wasted limb.

Old polio is uncommon in

nals and more common in post-

raduate exams.


8/16

4 WEEKS TO FINALS

36

Diagnosis: Median Nerve Palsy

GENERAL APPEARANCE: Usually normal

TONE: Reduced in thenar musclesPOWER: Reduced power of

flexion, abduction

and opposition of

the thumb

REFLEXES: Normal

SENSATION: Reduced over

palmar aspect of

the first three and

a half fingersCOORDINATION: Normal

OTHER: Wasting of the

thenar eminence

CAUSES: Compression of the median nerve as it runs

through the carpal tunnel is the most common.

NOTES: Carpal tunnel syndrome is caused by pregnancy,

rheumatoid arthritis, acromegaly, oral

contraceptive pill use, gout, TB and amyloid.Mononeuritis multiplex may also cause a median

nerve palsy (diabetes, SLE, sarcoid and other

inflammatory conditions). Diabetes may cause

a median nerve palsy without mononeuritis

multiplex.

P !

The commonest question about this

condition is the cause.

Ensure you look at the patient!

Does the patient have rheumatoid

hands? Do they look acromegalic?

Also ensure that you test fo

Tinels sign.

The median nerve palsy maynot be complete. There may just be

nsory loss.


9/16

NEUROLOGY CASES

37

Diagnosis: Radial Nerve Palsy

GENERAL APPEARANCE: Wrist drop

TONE: Decreased in wrist and finger extensorsPOWER: Reduced in wrist

and finger extensors

REFLEXES: Normal

SENSATION: May be some

reduced sensation

over thumb/dorsal

area between thumb

and 1st finger

COORDINATION: NormalCAUSES: Most common

cause is trauma to

the radial nerve as

it winds around the

spiral groove of the

humerus. Humeral fracture is therefore a common

cause.

NOTES: These patients present with wrist drop afterhumeral fracture or repair of a fracture. A gradual

return of function may occur. Swift repair of

the fracture may improve functional outcome.

Splinting of the wrist allows improvement of

function as the small muscles of the hand work

better with the wrist in the neutral position.

H E L !

You may not spot the wrist drop

traight away, as the patients

ands may be in the resting posi-

ion. Look for a splint nearby and

hen you examine the arm, look

or scars that suggest ortho-

aedic surgery for fracture.

If you ensure that you test allhe muscle groups, you will not

iss the diagnosis.

The commonest questions are

egarding cause and treatment.


10/16

4 WEEKS TO FINALS

38

Diagnosis: Ulnar Nerve Palsy

GENERAL APPEARANCE: Claw hand, wasting of the small muscles of the

handTONE: Decreased in small

muscles of the hand

POWER: Reduced/absent

power in the small

muscles of the hand

other than the

thenar muscles

REFLEXES: Normal

SENSATION: Decreased sensationin the little finger

and medial half of

the ring finger


OTHER: Hyperextended

MCP joints and flexed IPJs

CAUSES: Commonest is injury at the elbow (fracture,

lengthy surgery with pressure on nerve). Othercauses include mononeuritis multiplex (e.g.

diabetes, rheumatoid, SLE and others).

NOTES: Ulnar nerve injuries are obvious from the end of

the bed. Muscles affected are the small muscles of

the hand (other than the thenar eminence muscles),

flexor carpi ulnaris and the ulnar half of flexor

digitorum profundus.

H EL !

nsure you look for the cause..

ook for deformation at the elbow

oint as this is the commonest

ause. Also look for evidence

of diabetes (finger prick marks),,

rheumatoid changes (nodules) or

SLE (butterfly rash).

Treatment can involve reliev-ng any pressure on the nerve

(surgery), treatment of underly-

ing condition, or simple methods

h as s li t ng..


11/16

NEUROLOGY CASES

39

Diagnosis: Motor Neurone Disease 1

GENERAL APPEARANCE: May have contractures of both legs and visible

fasciculationTONE: Increased

POWER: Reduced

REFLEXES: Increased

SENSATION: Normal


OTHER: There may be ankle

clonus and up-going

plantars

CAUSES: Motor neuronedisease is a

degenerative

neurological

disorder of unknown

aetiology. There

is degeneration of

upper and lower motor neurones as well as cranial

nerve nuclei. This results in upper and lower motorneurone signs.

NOTES: Onset is usually after the age of 50. Men are

affected more than women. Most patients

die within 5 years. Prognosis is poor when

there are bulbar symptoms. Management is a

multidisciplinary approach with OT, physiotherapy

and speech therapy all being vital to maintaining

independence.

H E L !

The key to diagnosis in an exam

s the mixture of upper and lower

otor neurone signs and you

hould mention them. Questions

ou may get asked are around

iagnosis (clinical plus EMG)

nd management (seebelow).

The symptoms and signsre very variable depending on

hether upper or lower moto

eurone signs predominate.

Overleaf is an alternative clin-

cal picture.


12/16

4 WEEKS TO FINALS

40

Diagnosis: Motor Neurone Disease 2

GENERAL APPEARANCE: Cachexia

TONE: ReducedPOWER: Reduced (arms

and shoulders)

REFLEXES: Increased

SENSATION: Normal


OTHER: Wasting and

fasciculation seen

CAUSES: See previous page

NOTES: The alternativepresentation

is with bulbar

symptoms

wasted,

fasciculating

tongue, palatal

paralysis, and

indistinct nasalspeech. This

has the worst

prognosis of all

presentations.

H E P !

s can be seen, the presentation an

linical findings are very variable, but

iagnosis is easy when you divide the

ndings into upper and lower moto r

neurone.

The questions you need to ask

ourself when you examine any

patient neurologically are:Is this unilateral or bilateral?

(unilateral suggests brain lesion)

If bilateral, is there a sensory

level? (spinal cord)

If no sensory loss, is it upper or

lower motor neurone, or both?

(polio, MND)

If purely sensory, what tracts

are affected and are there

any pointers to the cause of aneuropathy? (finger prick marks)


13/16

NEUROLOGY CASES

41

Diagnosis: Multiple Sclerosis

GENERAL APPEARANCE: Very variable, usually a young patient, may be in a

wheelchair, may have contracturesTONE: Increased

(especially in legs)

POWER: Reduced

REFLEXES: Increased

(especially in legs)

SENSATION: Reduced

COORDINATION: Impaired, with

past pointing and

intention tremor.OTHER: Other cerebellar

signs may well

be present, optic

atrophy on

ophthalmoscopy,

possibly internuclear ophthalmoplegia

CAUSES: Plaques of inflammatory demyelination occur

anywhere within the CNS. The exact aetiology isunclear.

NOTES: The disease is diagnosed clinically by identifying

two or more neurological symptoms that are

separated in space and time. MRI demonstrates

plaques, and CSF analysis may show oligoclonal

bands. Assessment of visual evoked potentials can

aid diagnosis.

The condition is very variable in its course.

The variants are: relapsing remitting (majorityof patients), primary progressive, secondary

progressive, and fulminant. The commonest

presentation is with optic neuritis or sensory

symptoms.

Treatment with high dose steroids during a

relapse may help shorten the relapse, but they

do not affect long-term functional prognosis.

Few drugs have any effect in preventing relapsesalthough interferon beta may help in certain

groups (see NICE guidelines).3

H E L P !

The key in talking about MS in an

xam is to emphasise the need

or multidisciplinary management.

ome drugs can help reduce spas-

icity (baclofen or botulinum toxin) ,

ut physiotherapy is essential as

ell. OT assessment to improve

functionality in the home is alsovery important to talk about.

Mentioning the MS Society

and self-help groups always goes

n ll ith xamin rs..


14/16

4 WEEKS TO FINALS

42

Diagnosis: 3rd Nerve Palsy

GENERAL APPEARANCE: Unilateral ptosis

EYE POSITION: Affected eye is pointed down and laterallyMOVEMENTS: Unable to adduct the

eye past the midline

PUPIL: Dilated

OTHER: Patient almost

certainly complains

of double vision

when eyelid is

elevated

CAUSES: Commonest causeis microvascular

pathology, mostly

diabetes. This doesnt always result in the patient

having a ptosis or pupillary dilatation. Other

causes of a 3rd nerve palsy are cavernous sinus

lesions, superior orbital fissure lesions, vasculitis,

posterior communicating artery aneurysms (is the

palsy painful?). Mononeuritis multiplex may causethis (for which there are various causes).

NOTES: The patient should be investigated with a CT

scan of the head to look for structural lesions. A

vasculitis screen should be performed and a CXR

for sarcoid. Angiography for cerebral aneurysms

should be considered if the clinical picture suggests

this is likely.

H EL

As soon as you see the eye point-

ng down and out, you should

now the diagnosis. If there is

ptosis, ensure that you lift the

eyelid to check the position of

he eye.

You will get asked about caus-

es and possibly investigations.


15/16

NEUROLOGY CASES

43

Diagnosis: 6th Nerve Palsy

GENERAL APPEARANCE: Affected eye adducted

EYE POSITION: Inward pointing in the primary positionMOVEMENTS: No/limited

abduction of the eye

PUPIL: Normal

OTHER: Patient complains of

double vision when

attempting to abduct

the eye

CAUSES: Raised intracranial

pressure, MS,cavernous sinus

and superior orbital

fissure lesions, vascular lesions in the brainstem

NOTES: The 6th nerve has a long course. It is therefore

susceptible to damage from raised intracranial

pressure.

H E L !

s with the 3rd nerve palsy, the

ey is the eye position. If the

ye is adducted and unable to

bduct, you have the diagnosis..

IIf ophthalmoscopy reveals pale

ptic discs, the diagnosis is most

ikely to be MS. Papilloedema

ould suggest raised ICP.


16/16

4 WEEKS TO FINALS

44

Diagnosis: Diabetic Neuropathy

GENERAL APPEARANCE: May have Charcot joint, or ulcers

TONE: NormalPOWER: Usually normal

REFLEXES: Reduced ankle and

knee reflexes

SENSATION: Stocking (and glove)

distribution sensory

loss vibration sense

is the first modality

to go

COORDINATION: Normal, but gaitmay be wide based

or stamping

OTHER: Ulcers/callus

formation over

pressure areas

CAUSES: Diabetic neuropathy is relatively common and is

related to the degree of diabetic control as well as

duration of the disease.NOTES: Patients with diabetes should have their sensory

function tested yearly. They may complain of pain

(especially at night) in the feet and legs. Patients

should be advised to look after their feet and wear

well-fitting shoes.

A rarer form of diabetic neuropathy is

amyotrophy, which involves wasting and weakness

of the proximal muscles.

Complications of diabetic neuropathy includeneuropathic ulcers and Charcot joints.

H EL

The most likely diagnosis of a

sensory neuropathy in finals is

iabetes. The giveaway is finger

rick marks (if you get to see the

fingers!).

Ensure that you test all the

ensory modalities.

Questions would includemanagement of the neuropathy,

and management and monitor-

ing of diabetes and its other

omplications.

Neurology Cases

Documents

Transcript of Neurology Cases