Videos 2 Flashcards
Case: 47 y/o man with R cerebellar hemispherectomy secondary to large cerebellar stroke
Decreased coordination and fine-controlled movement as evidenced by FNF; movements choppy and slow, rapid alternating movements decreased in speed, difficulty with coordination of LE by heel knee shin, difficulty standing (unsteady) and walking (rigid uncoordinated steps)
Few months later - sleep slow and slurred, arm coordination improving, shaky in hand at times, R>L, unable to walk unassisted, can stand and walk with a walker, arm strength intact bilaterally
Ataxia due to bilateral PICA infarctions
What are the cardinal features of cerebellar dysfunction?
Disturbances in motor control, muscle tone regulation, coordination of skilled movements
May find ataxia, dysmetria, dysdiadochokinesia, impaired checking response, scanning/slurred speech, wide-based stance and gait
Arterial supply of the cerebellum?
PICA (from vertebral)
AICA, SCA (from basilar)
What does PICA supply?
Lateral medulla
Vermis, adjacent cerebellar hemisphere
Cortical surface of tonsil and cerebellar hemisphere
What does AICA supply?
Lateral tegmentum of the lower 2/3 of the pons
Ventrolateral cerebellum
Facial and auditory nerves
What does SCA supply?
Superolateral cerebellar hemisphere
Superior cerebellar peduncle
Dentate nucleus
Part of the middle cerebellar peduncle
Features of cerebellar infarction?
Severe vertigo, N/V, ataxia
Loss of balance, difficulty maintaing posture, standing, walking
Case - 31 y/o female, progressive history of gait and limb incoordination and head tremors
Bobbing, shaky head, trouble walking and speaking, difficulty getting words out, no difficulties swallowing, numbness/tingling in feet and mouth, family history of similar problems in mother and sister
Eyes remain stationary despite shaking head (intact VOR), difficulty writing due to shakiness, difficulty with fine motor movements, decreased coordination by FNF due to shaking, unsteady walk
Diplopia, abnormal EOM (esotropia), head and hand tremor, hypoactive reflexes, wide-based ataxic gait
Hereditary spinocerebellar ataxia
Features of spinocerebellar ataxia type 1?
Begins with gait ataxia
Develop dysarthria and dysphagia over time
Associated symptoms include ophthalmoparesis, spasticity, and choreoathetosis
Presentation: 44 y/o female, long history of neuro symptoms beginning in high school (1970s) - paraesthesias, dizziness, tiredness
1980 - acute onset vertigo, lower extremity weakness, fatigue
1996 - insidious onset of progressive difficulties with urinary incontinence, weakness, and poor balance
Currently - slight nystagmus looking laterally right; when looking left, L eye moves laterally but R eye remains central with slight nystagmus
Unsteady narrow gait, unable to turn sharply
Bilateral internuclea ophthalmoplegia 2/2 MS
Most common symptoms at the onset of MS?
Visual or oculomotor weakness or sensory disturbances and incoordination
What causes an INO?
Horizontal disconjugation gaze palsy
Paramedian pontine reticular formation (PPRF)
Abducens nucleus interneurons
To look left, the L lateral rectus (CN 6) and R medial rectus (CN 3) activate synchronously
Axons of CN 6 interneurons cross to contralateral side in lower pons and ascend to the MLF to the contralateral oculomotor nucleus
R INO = disrupted R MLF, poor adduction in R eye
Presentation of INO?
Adduction weakness of one eye and mononculear nystagmus of the abducting eye
Weakness results from disrupted signals carried by the MLF destined for CN III
Presentation: 27 y/o AA woman with several episodes of neuro deficits
First episode - marked fatigue, decreased vision, unsteadiness
Second episode - decreased vision in both eyes
Third episode - decreased vision, disequilibrium
Fourth episode - decreased vision, gait unsteadiness
Loss of balance for 2 weeks, blurred visino, eyes not focusing, R eye would move faster than L, right leg had abnormal temperature sensation, fatigue, nystagmus when looking R, superior, and inferior
Slow, unsteady, widened gait
Difficulty walking heel-to-toe
MRI: T2 signal in pons, mostly on the left, and bilateral subcortical white matter
Nystagmus and ataxia 2/2 relapsing-remitting MS
What is relapsing-remitting MS?
Most common form
Dysfunction occurs and may increase over days or week, plateaus, resolves over days or weeks
Presentation: following surgery of an intracranial mass lesion, 60 y/o F developed a droopy left eyelid and diplopia
L eyelid closed, L pupil unreactive to direct light, R pupil reactive to light directly, consensual constriction of R pupil when light shined in L eye, lateral L gaze intact, R eye moves lateral, L eye remains central look to the R; inferior and upserior -> R eye moves, L eye central/fixed
L eye ptosis, L eye extropia and hypotropia (down and out), anisocoria, no direct or consenusal L eye constrction
Post-operative acute L CN III palsy
Features of CN III palsy?
Eyelid ptosis
Pupillary dilation
Impaired pupillary reaction to light
Limitation of adduction, supraduction, infraduction
What does CN III innervate?
Levator palpebrae superioris, superior, inferior, and medial recti, inferior obliques, pupillary constrictors
Where can CN III lesions occur?
Midbrain (nucleus or fasciculus) Subarachnoid space Cavernous sinus Superior orbital fissure Orbit
Pathway of CN III?
Midbrain (rostral to CN IV nucleus) nucleus -> fascicular portion travels ventrally traversing the red nucleus, exits anteriorly medial to the cerebral peduncles
In the subarachnoid space, nerve passes between posterior cerebral and superior cerebellar arteries
Enters lateral wall of cavernous sinus
At superior orbital fissure, divides into superior division (levator palpebrae and superior rectus) and inferior division (medial and inferior recti, inferior oblique, pre-synaptic parasympathetic outflow)
Pupilloconstrictor is innervated by ___ system; dilator is innervated by ___ system.
Parasympathetic; sympathetic
What nerves are in the cavernous sinus?
III, IV, VI, V1, sympathetic and parasymapthetic connections
Blood supply to cavernous cranial nerves?
Arises from inferolateral trunk of the ICA and sometimes the accessory meningeal artery
CN III palsy associated with a small pupil?
Horner’s syndrome
What are signs of aberrant CN III regeneration?
Retraction and elevation of the lid on downward gaze
Elevation of the involved lid on attempted adduction
Retraction of the globe on attempted vertical eye movements
Adduction of the involved eye on attempted elevation or depression
Lack of pupillary reactivity to light, but adequate response when the medial rectus muscle, inferior rectus muscle, or elevators of the eye are activated
Delayed onset abduction defect
Case: 82 y/o male, history HTN, HLD, referred for evaluation of non-positional headaches and sudden onset binocular diplopia with horizontal separation of the images that were worse in the distance; no associated scalp or occipital tenderness, eyelid ptosis, history of thyroid disease, no diurnal variation of diplopia, no fatigability, no hx DM, sore shoulders or hips, jaw claudication
Exam: impaired abduction (LR) of R eye and nasal deviation (esotropia) of R eye in center gaze
Side-by-side double vision, worse when looking right and straight ahead, separation of images worse when looking right and far vs. right and near, some nausea and lightheadedness
R eye remains more central and fixed while L eye is turned slightly inward, decreased lateral movement of R eye (more central) compared to normal L eye when looking right. Left lateral, superior, and inferior gaze intact for both eyes
MRI: changes compatible with small vessel ischemic disease; no brainstem acute changes on DWI
MRA - minimal tortuosity of vertebrobasilar system
CN VI palsy
Pathway of abducens nerve?
Nucleus located in dorsal lower pons, exits brainstem ventrally at the level of the horizontal sulcus between the pons and medulla, courses anterolaterally passing over the petrous apex to enter the lateral wall of the cavernous sinu
Enters the orbit through the superior orbital fissure with CN III and IV
Most common cause of CN VI palsy in older adults?
Microvascular occlusion of the nerve; most recover over a period of 3-6 months
Case: 57 y/o male evaluated because of a 3-4 month history of progressive unilateral sensorineural hearing loss and subjective nonpulsatile tinnitus of the R ear
MRI: internal auditory canals demonstrating a small enhancing mass
Small R vestibular schwannoma
If bilateral vestibular schwannomas, suspect what condition?
NF2
Cause of autonomic signs in cluster headache?
Sympathetic paresis and parasympathetic overactivity
Rx cluster headaches?
High-flow concentrated oxygen (acute)
Verapamil (#1), ergotamine, lithium carbonate, methysergide, prednisone, depakote, topiramate (prophylactic)
Presentation: 31 y/o obese normotensive female with long-standing headaches, visual scotomata, bilateral papilledema, enlarged blind spots on visual field testing
Remainder of exam was unremarkable
Neuroimaging - normal brain MRI and MRV (excludes mass, cerebral venous thrombosis)
LP elevated opening pressure, normal CSF
Pseudotumor cerebri
Diagnostic criteria for pseudotumor cerebri?
- Signs and symptoms of increased ICP (headaches, transient visual obscurations, and horizontal diplopia due to unilateral or bilateral CN VI palsy)
- Normal neuroimaging (MRI and MRV preferably)
- Increased opening CSF pressure (>250) with normal composition
Rx papilledema?
Weight loss if overweight
Diuretics like acetazolamide or furosemide
Most common seizure type in adults? Most common site of epileptogenic focus?
Complex partial seizure
Temporal lobe (medial temporal lobe)
What aspects of a seizure may indicate a contralateral epileptogenic region?
Forced and sustained head deviation and dystonic posturing of the upper extremity
What aspects of a seizure may indicate an ipsilateral focus?
Unilateral upper extremity automatisms
What indicates a dominant-hemisphere seizure?
Post-ictal dysphagia
