Neuro Review (Jersey)

7/27/2019 Neuro Review (Jersey)

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Neuroanatomy Review for

USMLE Step 1



Meningeal dura

Periosteal dura

Meninges• Dura Mater – Tough membrane of cranial cavity; composed of 2 layers (does NOT continue with spinal dura)

• Periosteal (Endosteal) Dura – Outer layer forms periosteum…fuses to bone at sutures • Middle meningeal artery is primary blood supply to dura & runs in this layer • Fracture produces EPIDURAL hematoma (limited by sutures) & IMMEDIATE headache• Puts pressure on underlying portion of brain…affects OPPOSITE side of body

• Meningeal (Internal) Dura – Inner layer…sends 4 partitions (i.e., falx cerebri) that encase brain • CONTINUOUS with dura covering spinal cord & cranial nerves• Most dural sinuses are situated between the 2 layers of dura & are lined by endothelia• Tearing cerebral veins produces SUBDURAL hematoma & DELAYED symptoms (contralateral, upper body)

• Subdural space – Between meningeal dura & underlying arachnoid membrane (note: we’re OUTSIDE the arachnoid space!) • Arachnoid Mater – Avascular membrane covers brain but does NOT dip down into sulci; continuous with spinal arachnoid

• Goes over arachnoid granulations & sends out spider web-like trabeculae that connect to underlying pia mater • Pia Mater – Dips down into sulci & cannot be separated from brain (also covers arachnoid granulations)• Subarachnoid Space (SAS) – Contains cerebrospinal fluid (CSF) & is continuous with spinal pia

• Cerebral & spinal vessels pass thru here…rupture produces SUBARACHNOID hematoma

• Symptoms are “thunderclap” headache & history of vomiting, disturbed vision, etc. before rupture

Diploae(spongy bone)



Lesion Here Motor aphasia• Broca’s broken speech motor • You can understand other people• You can’t articulate words properly

Lesion Here Sensory aphasia• Wernicke’s wordy people • You babble incessantly• You don’t understand a word • Nonsensical streams of words

Lesion Here Major personality changes• Connects to DM nucleus of thalamus• Related to limbic system (emotion)• Concentration, reasoning, spontaneity, social norms

Lesion Here Conductive Aphasia• Connects Broca’s & Wernicke’s areas • Cannot repeat words/phrases• Substitutes words or changes order



Lesion Here IPSILATERAL deviation• Normally, stimulation causes contralateral

eye to deviate to side of stimulation• Enables conjugate eye movements; lesions

impair voluntary aversive eye movements

Lesion Here Dyskinesia• Execution of movements

Lesion Here Akinetic mutism• Plans/programs voluntary movements• General paucity of spontaneous movement & speech

Frontal Eye Fields (FEF)(deep to middle frontal gyrus)• Conjugate eye movements

Lesion Here CONTRALATERALHomonymous Hemianopsia

• Loss of entire visual field



Lesions of Lower MedullaLesions of Posterior Column System

Anterograde degeneration of IPSILATERALFG or FC (T6+) depending on spinal levels

IPSILATERAL loss of tactile sensation &kinesthesis for those spinal levels

Unilateral Dorsal Rhizotomy




Unilateral Lesion of NG or NC

IPSILATERAL loss of tactile sense & kinesthesisFor lower trunk & extremity (NG = T7 – S5)

Anterograde degeneration of IPSILATERAL arcuate fibers

Nucleus Cuneatus

Nucleus Gracilis

IPSILATERAL loss of tactile sense & kinesthesisFor UPPER trunk & extremity (NC = C1 – T6)

Anterograde degeneration of IPSILATERAL arcuate fibers




Anterograde degeneration of IPSILATERALmedial lemniscus ABOVE level of lesion

CONTRALATERAL loss of tactile sensation &kinesthesis

Unilateral Lesion of Medial Lemniscus (ML)



Lesions of Lower MedullaLesions of Trigeminal System

Unilateral Lesion of Spinal V Tract and/or Nucleus

Loss of pain, light touch, & thermal sensation inIPSILATERAL face

Unilateral Damage of Trigeminothalamic fibers

Loss of pain, light touch, & thermal sensation inCONTRALATERAL face

Remember, neurons of spinal V nucleus emit fibers that form the trigeminothalamic tract.The tract then CROSSES in brain stem & ascends to the thalamus.



Lesions of Upper MedullaClinical Name: Inferior Alternating Hemiplegia

Cause:

Pathways involved: Upper Motor Neuron (UMN)& Lower Motor Neuron (LMN) pathways

Vascular disturbances of anterior spinal artery(i.e., stroke, trauma, etc.)

UMN damage to ___ tract(s)? Pyramids

Symptoms: Paralysis to CONTRALATERAL side of body

UMN Damage Symptoms, incl. Babinski’s sign (hyperreflex, hypertonia, slow atrophy, etc.)

LMN damage to ___ tract(s)? XII nucleus

Paralysis of IPSILATERAL tongue musclesTongue deviates to side of lesionRapid atrophy of muscles (hypotonia)

Symptoms:



LOWER MOTOR NEURON LESIONS UPPER MOTOR NEURON LESIONS

• CAUSES: CAUSES:• •1) Degeneration of Anterior Horn Cells 1) Degeneration of Nerve Cell Bodies in•2) Transection of Ventral Roots the Motor / Somatosensory Cortices•3) Transection of Spinal Nerves 2) Damage to Axons of Descending

Systems particularly CorticospinalFibers

• • SYMPTOMS: SYMPTOMS:

•1) Flaccid Paralysis 1) Spastic Paralysis•2) Loss of Myotatic Reflexes 2) Hyperactive Myotatic Reflexes•3) Hypotonia 3) Hypertonia

•4) Muscle Fasciculations 4) Clonus•5) Atrophy of Denervated Muscles 5) Muscle Atrophy--if it occurs, it is very

late and results from disuse• 6) Babinski Sign (Corticospinal Damage)• 7) Loss of Superficial Abdominal Reflex

and Cremasteristic Reflex (males)



Neurological Disorders of Brain StemSYNDROME STRUCTURES DAMAGED CLINICAL SYMPTOMS

Corticospinal Tract Contralateral hemiparesis

Lower motor impairment of ipsi lateral tongue

(Tongue deviates to side of lesion)

Inferior AlternatingHemiplegia

Damage Level:Ventral Medulla

Middle AlternatingHemiplegia

Damage Level:

Ventral Lower Pons


Lower motor impairment of ipsilateral lateral rectus m.

(Internal strabismus – ipsilateraleye is crossed)

Corticobulbar Tract Contralateral paralysis of

lower face

• Corticobulbar symptoms are usually only seen for the contralateral lower face region.

• Symptoms from impairment of corticobulbar inputs to CN V & XII, & inputs for innervation of the upper faceare NOT observed due to BILATERAL corticobulbar inputs to these cranial nerve nuclei.

Abduscens Nerve ( VI )

Hypoglossal Nerve ( XII )



Neuro Disorders of Brain Stem (Con’t.) SYNDROME STRUCTURES DAMAGED CLINICAL SYMPTOM

Superior AlternatingHemiplegia

Damage Level:Ventral mesencephalon;usually due to vascular disturbance inposterior Circle of Willis

Also called:Weber’s Syndrome


Ipsilateral paralysis of oculomotor nerve

(Down & Out – eyelid is down& eye deviates outward)

Corticobulbar Tract Contralateral paralysis of lower face muscles



Note how each syndrome involves damageto one of the “3X” cranial nerves:

(CN III, VI, IX, and/or XII)Corresponds to the level of the lesion

Oculomotor Nerve (III )




Millard-Gubler Syndrome

Damage Level:Ventral & Lateral Pons

Corticospinal Tract

Abduscens Nerve (VI)

Contralateral hemiparesis

Lower motor impairment of ipsilateral lateral rectus m.

(Internal Strabismus)

Corticobulbar Tract Contralateral paralysis of lower face



Facial Nerve (VII) Ipsilateral lower motor impairment of entire face

Loss of corneal reflex(direct & indirect)



Neuro Disorders of Brain Stem (Con’t.) DAMAGE CLINICAL TEST CLINICAL SYMPTOM

Optic Nerve (II)Lesion, Left Side

Light shown inLEFT eye

Light shown inRIGHT eye

NO direct pupillary lightreflex in LEFT eye

Direct pupillary light reflexin RIGHT eye

NO consensual pupillaryreflex in RIGHT eye

Consensual pupillary lightreflex in LEFT eye

Lesion toLeft Optic N.

What Did You Kill? All SENSORY input

to the brain

What is Left Intact? All MOTOR controlby the brain ( CN III )

• Damage to LEFT eye:• DIRECT reflex lost on side of lesion• CONSENSUAL reflex also lost in right eye

• No sensation in left eye• Right eye can still move just fine, but… • No message gets to brain to let it know light is on left side

• If you shine a light in the RIGHT eye:• Sensory input now comes from opposite (undamaged) side• Motor control is intact to left side, so consensual reflex intact



Neuro Disorders of Brain Stem (Con’t.) DAMAGE CLINICAL TEST CLINICAL SYMPTOM

Oculomotor Nerve (III)Lesion, Left Side

Light shown inLEFT eye

Light shown inRIGHT eye

NO direct pupillary lightreflex in LEFT eye

Direct pupillary light reflexin RIGHT eye

Consensual pupillaryreflex in RIGHT eye

NO consensual pupillarylight reflex in LEFT eye

Lesion toLeft Optic

Tract

• Damage to LEFT eye:•DIRECT reflex lost on side of lesion• Consensual reflex lost w/light shown in right eye

• Notice that the RIGHT eye is unaffected• Brain senses light but commands can’t get to the muscle

What Did You Kill?

All SENSORY inputto the brain ( CN II )

What is Left Intact?

All MOTOR controlby the brain ( CN III )




Oculomotor NervePalsy

Damage Level:Lesion of CN III(Oculomotor n.)

Lower Motor Neuron

Extrinsic eye muscles:• Sup, Medial, Inf rectus• Inferior oblique

Ipsilateral LMN paralysis of muscles supplied by III

Lateral deviation of

ipsilateral eye (externalstrabismus); unopposedaction of lateral rectus m.

Ipsilateral ptosis (can’traise eyelid); paralysis of levator palpebrae m.

Pupil Ipsilateral dilation of pupil

Levator palpebrae m.

Ipsilateral loss of pupillarylight reflex & accomodation




Tegmental (Benedikt’s) Syndrome

Damage Level:Lateral tegmental infarct

Red Nucleus

Medial Lemniscus

Cerebellar symptoms inContralateral limbs

(intention tremor & ataxia)

Contralateral loss of 2-pt.tactile discrimination &pain & thermal sensation

Superior Cerebellar Peduncle

Spinothalamic Tracts

Oculomotor Nerve (III)(courses thru red nucleus)

Ipsilateral occulomotor nerve palsy

Cerebellar symptoms inContralateral limbs

(intention tremor & ataxia)

Contralateral loss of 2-pt.tactile discrimination &pain & thermal sensation




Collicular (Parinaud’s) Syndrome

Damage Level:Superior colliculus dueto vascular disturbance

or pineal tumor

Structures inReticular Formation

Paralysis of vertical upwardor downward gaze;direction of which dependson level of lesion



Peripheral Facial Nerve PalsiesLOCATION OF LESION FIBERS DAMAGED CLINICAL SYMPTOM

As Nerve ExitsStylomastoid Foramen

SVE fibers to musclesof facial expression;

post. digastric &stylohyoid muscles

Paralysis of muscles of ipsilateral face

Corneal sensation persists(Trigeminal nerve V intact)

Ipsilateral loss of cornealreflex

Nerve to stapedius intact(hearing unimpaired)

What functions remain?(i.e., what is NOT damaged?)

GVE to salivary glandsintact

SVA to taste intact

Clinical Signs of Muscle Paralysis• Ipsilateral face sags (e.g., corner of mouth droops)• Normal lines around eyes, mouth, etc. “ironed out” • Corner of mouth drawn to side opposite of paralysis when patient smiles• Saliva may ooze from lips on paralyzed side• Laceration of inside cheek when chewing & cheek may puff out with

expiration on paralyzed side (buccinator denervated)• Dry eyes (inability to shut eye produces tears & corneal irritation)

Lesion A

*Also called :Bell’s Palsy



Peripheral Facial Nerve Palsies (Con’t.) LOCATION OF LESION FIBERS DAMAGED CLINICAL SYMPTOM

Distal to GeniculateGanglion

(in posterior wall of middle ear cavity)

Lacrimation intact






SVE fibers to stapedius Ipsilateral hyperacusis

Taste (SVA) fibers inchorda tympani

Ipsilateral impaired tastesensation for anterior 2/3of tongue

Parasympathatic fibersin chorda tympani

Ipsilateral impairment of salivary secretion

Lesion B



Peripheral Facial Nerve Palsies (Con’t.) LOCATION OF LESION FIBERS DAMAGED CLINICAL SYMPTOM

Proximal to GeniculateGanglion

(in internal auditory meatus)&

Facial Nerve in Lower Pons

Nothing…this jacks it all





SVE fibers to stapedius Ipsilateral hyperacusis

Taste (SVA) fibers inchorda tympani

Ipsilateral impaired tastesensation for anterior 2/3of tongue

Parasympathatic fibersin chorda tympani

Ipsilateral impairment of salivary secretion

Parasympathatic fibersto lacrimal gland

Ipsilateral impairment of lacrimal secretion (dry eye)Lesion C




Peripheral Facial Nerve PalsiesLOCATION OF LESION FIBERS DAMAGED CLINICAL SYMPTOM

Facial motor nucleusin lower pons




Corneal sensation persists


Ipsilateral hyperacusis



UMN versus LMN LesionsUMN Lesion (A)

With an upper motor neuron (UMN) lesion, theupper face is spared because both hemispherescontribute to movement of the upper face & theunaffected hemisphere can compensate.• Such lesions involve face area of primary motor

cortex or descending corticobulbar fibers• Called CENTRAL FACIAL PALSY or

CORTICOBULBAR PALSY

LMN Lesion (B)With a lower motor neuron (LMN) lesion, theentire face is affected on one side.• Such lesions involve the motor facial nucleus

or facial nerve in pons, cranial cavity, middle

cavity or on its course of peripheral distribution• Called PERIPHERAL FACIAL PALSY or LMN FACIAL PALSY



Central Facial PalsyVoluntary Central Facial Palsy• Paresis (weakness) of contralateral lower face muscles• NO impairment of emotional facial expression (i.e., SYMMETRICAL smile)• NO paresis of upper face muscles on either side due to bilateral input• NO loss of corneal reflex

Mimetric Central Facial Palsy• Paresis (weakness) of facial muscles only in response to emotional stimuli (i.e., ASYMMETRICAL smile)• NO impairment of voluntary facial expression• Unknown pathway but different from that for voluntary facial expression

Corticospinal System• Axons of UMN in primary somatosensory & motor cerebral cortex form descending corticospinal fiber tracts• Corticospinal fibers synapse directly or via interneurons on Lamina IX α motor neurons in spinal cord

• LMN in Lamina IX project axons in ventral roots, thru spinal nerves to skeletal muscles (final pathway)

Corticobulbar Fibers• Motor nuclei of cranial nerves & their cranial nerves constitute LMN to skeletal muscle of neck/face region• UMN from facial area of primary motor cortex descend & synapse directly on cranial motor nuclei V, VII, XII

• Usually in close proximity to corticospinal fibers damage to one usually means damage to both• Corticobulbar fibers to motor nuclei of V & XII are bilateral loss of one produces no clinical effect• Corticobulbar fibers to motor nucleus of VII also bilateral but different for upper & lower face

•Neurons in face area of primary motor cortex project corticobulbar fibers to facial motor nucleus (VII)• Those innervating upper face are BILATERAL• Those innervating lower face CROSS in lower pontine tegmentum at level of motor nucleus VII

• Midbrain or basilar pons lesion produce contralateral lower face & limb paralysis (Central Facial Palsy)

• Both corticospinal & corticobulbar tracts usually involved since they travel together • Bilateral input from cortex to upper face motor neurons enables unaffected side to compensate



SMA Cortex

GABA/Sub P

GLUT

GABA

GABA

GABA/

ENK

GLUT

Basal GangliaLesions

DOPA

MPS & SNr

VA/VL nucleiof thalamus

Cortex

Substantia Nigra,Pars Compacta (SNc)

SubthalamicNucleus

LPSStriatum

A

B

C

Loss of A Huntington’s Disease

Loss of B Ballism

Loss of C Parkinson’s Disease



Basal Ganglia Lesions Produce:• HYPERkinetic disorders – Huntington’s Disease & ballism (uncontrolled involuntary movements)

• Loss of GABA-enkephalin striatal neurons Huntington’s (chorea, hypotonia, dementia) • Loss of STN Ballism (forceful flinging movements of extremities)• Decreased activity in INDIRECT pathway (normal suppression no longer there)

• HYPOkinetic disorders – Parkinson’s Disease• Characterized by rigidity, dystonia, resting tremor, slow, & difficulty initiating movement• Loss of dopamine producing cells in substantia nigra pars compacta• Decreased activity in DIRECT pathway (tough to get the motor started)

Basal Ganglia Lesions



CEREBELLAR LESIONSSYNDROME STRUCTURES DAMAGED CLINICAL SYMPTOM

Medulloblastoma(Brain tumor

affecting children)

Also called Posterior Vermis Syndrome

Damage Level:

Midline lesion affectingvermis &/or fastigial nuc.

Vestibulocerebellum(Nodulus)

Ataxic gait (drunk walk)

Nystagmus (inability to makesmooth eye movements)

Head tremor (inability tostabilize head)

What position relievesthese symptoms?

Recumbent position

Symptoms reflect inabil i ty to con t ro l t runk m usc les

according to gravity(truncal dystaxia )

Why?

General Principles:• Ataxia is IPSILATERAL to the side of the cerebellar lesion• Midline lesions of vermis or flocculonodular lobes cause:

• Unsteady gate (truncal ataxia) & eye movement abnormalities• Often accompanied by intense vertigo, nausea, & vomiting

• Lesions lateral to vermis cause ataxia of limbs (appendicular ataxia)• May be combined w/other lesions due to connections to CNS regions



CEREBELLAR LESIONS (Con’t.) SYNDROME STRUCTURES DAMAGED CLINICAL SYMPTOM

AlcoholicDegeneration

Also called Anterior Vermal Syndrome

Damage Level:Midline lesion affecting

rostral vermis of anterior lobe

Spinocerebellum(Vermal portion)

Truncal ataxia (unsteady gait)

Does a recumbentposition also relievethese symptoms?

NO!Symptoms don’t improve

Symptoms reflect inabilitygenerate mo tor p at terns

of walking

Why?

Do cerebellar lesions EVER cause paralysis?NO!!

Cerebellum only influencescontrol of our muscles



Cerebellar Lesions (Con’t.) SYNDROME CLINICAL SYMPTOM

Hemispheric Lesions

Causes:Numerous; includingtumors, stroke, MS

General Damage Asynergia (disorderedmovement) of Ipsilateral limbs

Intention tremor (occurs onlyduring attempted movement)

Typical Symptoms

Gait ataxia

Dysmetria (errors in distancesof movement…over/undershoot)

Dysdiadochokinesis (difficultymaking repetitive agonist/antag-onist movements)

Decomposition of movement(complex moves broken downinto individual components)

Speech problems ( dysarthria

& scanning /no inflection speech)

P i Vi l P h



Primary Visual Pathways

Optic Nerve (CN II)• Retina develops from diencephalon optic n. is part of CNS• Surrounded by meninges• Subarachnoid space of brain continuous along the nerve• Each optic nerve contains axons of all ganglia in ipsilateral retina

Optic Chiasm• Partial decussation of fibers• Fibers from nasal halve of each retina cross over • Each tract contains:

• Fibers from temporal (lateral) retina of IPSILATERAL eye

• Fibers from nasal (medial) retina of CONTRALATERAL eye• Pay careful attention to which visual field each retina receives!• Visual stimuli from one half visual field processed in contralateral brain

Lateral Geniculate Body• Each layer of LGB receives MONOCULAR input• Most fibers from optic tract end here

• CROSSED fibers end in layers 1 + 4 ≠ 6 (from contralateral eye)• UNcrossed fibers end in layers 2 + 3 = 5 (from ipsilateral eye)

Brachium of Superior Colliculus• Fibers ending in superior colliculus identify & track moving targets

• Efferent (output) tract of PULVINAR• Fibers in pretectal area mediate pupillary light reflexes

** Where does BINOCULAR INPUT occur? ONLY in visual cortex! **• First place where fibers carrying info from both eyes converges

L i i P i Vi l P h



Lesions in Primary Visual Pathways

Neuro Review (Jersey)

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