Neuro Flashcards
Causes of CN I (Olfactory Nerve) Palsy
Causes of CN I palsy
- Head injuries due to shearing of olfactory nerve filaments or fracture of the cribiform plate
- Frontal lobe tumour or abscess
- Ethmoid tumours
- Meningiomas of olfactory groove
Finding in CN I (Olfactory Nerve) Palsy?
Anosmia
Explain the difference in findings between pre-chiasmic, chiasmic and post-chiasmic CN II (Optic N) lesions?
Pre-chiasmic: Unilateral blindness, unilaterally unreactive pupil (but the pupil would react with the consensual pupillary reaction)
Chiasmic: Bitemporal hemianopsia
Post-chiasmic: Homonymous hemianopia or quadrantanopia depending on location of the lesion
Causes of prechiasmic CN II lesions (CN II = Optic nerve)
of sphenoid bone (transecting the optic nerve)
Retinal tumors
Masses compressing the optic nerve
Causes of lesions at CN II chiasm (CN II = Optic nerve)
Pituitary adenoma
Craniopharyngioma
Saccular Berry aneurysm at optic chiasm
Causes of post-chiasmiatic lesions
Stroke
Anterior choroidal artery infarction
Multiple sclerosis (or other demyelinating disease)
Trauma
Internal capsule stroke (eg. basilar artery)
Haemorrhage
MCA stroke (lenticulostriate arteries)
PCA stroke
PRES (posterior reversible encephalopathy)
What are the expected findings of a prechiasmatic CN II (Optic) lesion?
Unilateral blindness and unilaterally unreactive pupil
What are the expected findings in a CN II (Optic) chiasma lesion
Bitemporal hemianopsia
What are the expected findings in a postchiasmatic CN II (optic) nerve lesion?
Homonymous hemianopia or quadrantanopia depending on the location of the lesions
+/- Macular sparing (Occipital cortex)
What are the expected findings in a CN III (Oculomotor) nerve lesion?
Ptosis (inferolateral displacement of the ipsilateral eye)
Dilated non-reactive pupil (to contralateral light reflex and accommodation) [note, Argyll Robinson Pupil accommodates but does not react]
What are the causes of CN III palsy (CN III = Oculomotor)
Diabetes (pupillary sparing)
Other causes of mononeuritis
Midbrain lesion, vascular, demyelinating
Basilar skull fracture
Uncal herniation as a result of increased intracranial pressure
SOL in the cavernous sinus
Syphilis (argyll Robinson)
Aneurysms (post communicating artery)
What are the expected findings in CN IV (Trochlear) palsy?
Weakness of downward eye movement with consequent vertical diplopia that is worse in the adducted eye position, but improved diplopia with head tilted to contralateral side
Weakness of intorsion, in particular with the eye abducted
What are the causes of CN IV (Trochlear) lesion?
Diabetes (mononeuritis)
Fracture of the sphenoid wing
Intracranial haemorrhage
Aneurysm (post communicating artery)
Midbrain lesion, vascular, demyelinating
Masses or tumours in the cavernous sinus
What are the expected findings in a CN V palsy?
Sensory abnormality
- Peripheral nerve OR
- Brain stem distribution
Motor abnormality:
- Asymmetry of jaw on opening or weakness with mastication
What are the causes of CN V (Trigeminal) lesion?
Trauma with skull fracture
Pontine lesions, vascular, demyelinating, tumour in pons and cerebellopontine angle eg. acoustic neuroma
Facial surgery - disturbance of peripheral branches of the sensory component
Cavernous Sinus lesions (upper 2 segments)
What are the expected findings of CN VI (Abducens) palsy
Medial deviation of ipsilateral eye
What are the causes of CN VI (Abducens) lesion
Wernicke’s (unilateral or bilateral)
Mononeuritis
Lesions in the cavernous sinus
Fractures of skull base
Raised intracranial pressure
Lesions in pons (vascular or demyelinating), cerebellopontine angle (eg. acoustic neuroma)
Idiopathic
What is the most common cause of CN palsy?
Diabetes
Other possibilities include:
- Aneurysm
- Vascular event
- Mass lesion
Describe internuclear ophthalmoplegia?
Due to a lesion in the medial longitudinal fasiculus (heavily myelinated tract that runs between CN III and CN VI)
Findings:
- Ipsilesional adduction deficit (partial or complete)
- Contralateral, dissociated, horizontal abducting saccade/nystagmus on attempted gaze to the contralesional side.
- Slow adducting saccadic velocity in the affected side.
- Skew deviation with the ipsilateral hypertropic eye may be noted.
- Vertical gaze nystagmus may be noted on upgaze.
- The INO can be unilateral or bilateral and may present with or without (neurologically isolated) other brainstem findings.
Causes of horizontal gaze palsies
- Frontal lobe lesions: deviation of eyes away from hemiparetic side and towards affected hemisphere
- Pontine gaze centre lesions: deviation of eyes towards the hemiparetic side, contralateral to the pontine lesion
Causes of complex ophathlmoplegia
Myasthenia
Graves eye disease
Mitochondrial myopathies
Which nerves are involved in cavernous sinus lesions
Sympathetic
CN III
CN IV
CN V (ophthalmic and sometimes maxillary divisions)
CN VI
Carotid artery
Ophthalmic veins
Causes of cavernous sinus lesions?
Metastatic tumors
Localized spread of tumor: nasopharyngeal, pituitary
Primary intracranial tumors: meningiomas, neurofibromas
Carotid artery aneurysm
Carotid-cavernous fistula
Cavernous sinus thrombosis Eg. Bacterial, secondary to sinusitis, facial cellulitis
Miscellaneous inflammatory syndomres: Sarcoidosis, fungi/parasites (immunocompromised)
Features of Myotonic Dystrophy?
- *Muscle**
- Myotonia (slow relaxation of hand grip, becomes less with muscle atrophy)
- Weakness of: Distal > Proximal
- Neck muscles (flexors and sternocleidomastoid)
- Distal limb muscles, intrinsic muscles of hand, foot (foot drop)
- Proximal usually stronger, but in some selective atrophy and weakness of quadriceps
- Palatal, pharyngeal and tongue involvement, swallowing and speech problems, dysarthria and nasal speech
- Diaphragmatic and intercostal muscle involvement may cause respiratory problems
- Subgroup with proximal weakness
- *Facial features:**
- Frontal baldness
- “Hatchet face” due to temporalis, masseter and facial muscle weakness and atrophy
Other:
Cardiac: Conduction problems, CHB; CCF; MVP
Intellectual impairment
Cataracts (multicoloured)
Drowsiness
Insulin resistence
Gonadal atrophy
Oesophageal and colonic reduced motility
Parkinson’s disease - examination
Gait
Stooped, small steps, festinated, loss of arm swing, difficulty turning
Loss of balance (pull test)
Upper limbs
Hand tremor: resting, coarse, pill-rolling, asymmetrical. Improves with intention worsens when walking.
Bradykinesia: Progressive reduction in amplitude of movements, Eg. touch thumb to each finger (Decrementing movements), piano fingers, open/close fists
Primitive reflexes: Palmar-mental; grasp reflex
Head/Face
Mask-like face
Glabellar tap
Eye movements, saccades (PSP), gaze palsy
Other: voice, micrographia, postural BP, MMSE
Parkinson plus - how to differentiate from PD?
PSP (Eye signs - saccades, gaze palsies)
MSA (Autonomic dysfunction, do a postural BP)
What is the clinical significance of Pes Cavus?
- Pes Cavus is due to atrophy of the intrinsic muscles of the feet
- Appearance = high arch, claw toes, feet look thicker
- Causes:
- CMT (Hereditary motor and sensory neuropathy)
- Friedreich’s
- Other spinocerebellar degenerative disease
- Childhood neuropathies, spina bifida
- Idiopathic
UMN findings with upper and lower limbs affected
Unilateral
Sensory findings present
What is the ddx?
Stroke/Central lesion/Cortical/subcortical
Brainstem
Spinal cord (Brown Sequard)
UMN findings with upper and lower limbs affected
Bilateral
With sensory findings
Spinal cord compression (look for sensory level. Arms = cervical level)
MS (sensory findings variable, may have cerebellar findings)
B12 deficiency
Multiple CVAs
Arnold Chiari malformation (will also have cerebellar signs)
UMN findings
Upper and lower limbs affected
Bilateral
No sensory findings
Cerebal palsy
MND (should see mixed UMN and LMN)
Multiple CVAs, often lacunar
UMN findings
Lower limbs only (upper limbs normal)
Cerebral palsy (may selectively affect lower limb fibres)
Spinal stenosis below cervical spine
Parasagittal tumours, meningiomas
Hydrocephalus
Hereditary Spastic Paraparesis (sensory findings often mild)
UMN signs
+ Ataxia
+/- sensory findings
Spinocerebellar degeneration
MS
Ataxic hemiparesis (lacune in upper pons/internal capsule)
Arnold Chiari Malformation
LMN findings
No sensory loss
Polio Kennedy syndrome
LMN findings
Sensory loss
Peripheral nerve
Nerve root compression
Cauda equina syndrome
Plexopathies
Peripheral neuropathies (sensorimotor)
LMN peripheral neuropathy f
Areflexia
Distal weakness
Patchy sensory loss
Acute Guillian Barre
CIDP
Heredeitary neuropathy (CMT)
LMN peripheral neuropathy
Areflexia
Sensory involvement
Little motor loss
Diabetes
Alcohol
Drugs eg. Vincristine
CKD
Paraneoplastic
Vit B12 deficiency
Differentials for absent ankle jerk and upgoing plantar
MND (UMN and LMN findings)
Dual pathology - peripheral neuropathy and UMN lesion (sensory findings)
Friedreich’s Ataxis
Subacute combined degeneration (B12 deficiency)
UMN signs
Spastic tone
Hyperreflexia
Positive Babinski
No atrophy
No fasciculations
LMN signs
Flaccid tone
Atrophy present
Absent reflexes
Absent Babinski
Fasciculations present
What are the causes of positive Romberg’s test?
- Posterior column lesion
- Peripheral neuropathy (especially affecting JPS)
- Vestibular dysfunction (associated with ataxic gait)
What are the expected LL neuro findings in diabetic peripheral neuropathy?
Bilateral distal sensation loss in a stocking distribution.
Absent ankle jerk
Romberg +ve (not always)
Sensory ataxic gait
What are the expected LL neuro findings in CIDP?
Symmetrical sensorimotor neuropathy
Distal + proximal involvement
Romberg +ve (not always)
Reflexes absent
Muscle atrophy
What are the expected LL neuro findings in multiple sclerosis?
Predominantly motor UMN findings:
Hyperreflexia (though reflexes may be lost due to interruption of motor reflex arc fibres)
Spasticity
Up-going plantar
+/- cerebellar findings
+/- sensory (patchy)
What are some differential diagnoses for a bilateral symmetric spastic gait?
Bilateral stroke
Hereditary Spastic Paraplegia (HSP)
Spinal cord lesion
Cerebral palsy
Multiple sclerosis
What are some differential diagnoses for bilateral foot drop
Peripheral sensorimotor neuropathy eg. CIDP, Charcot Marie Tooth
Bilateral strokes
Motor neuron disease
What are some differential diagnoses for Parkinsonian-like gait
Parkinsonism: shuffling gait, stooped posture, loss of arm swing, tremor
Parkinson like syndromes: PSP, drug induced parkinsonism (posture upright)
What are the differential diagnoses for wide-based gait?
Cerebellar ataxia
Sensory ataxia
Vestibular ataxia
Frontal ataxic gait (unlikely in exams)
What are the likely causes for an asymmetric gait?
Unilateral spasticity eg. motor stroke
Unilateral cerebellar lesions
Unilateral foot drop (eg. Common peroneal nerve lesion, L5 lesions, unilateral stroke)
Which conditions are pes cavus seen in?
Charcot Marie Tooth
Friedrich’s Ataxia
Which nerve roots are responsible for knee and ankle reflexes?
Knee: L3, 4
Ankle: S1, 2
