question

What is the clinical utility of CT and MRI?

answer

*CT* is best used to identify fresh blood *MRI* in general is better than CT for deeper brain structures such as the posterior fossa and craniocervical junction. *DWI MRI* is best used to catch early tissue ischemia, i.e. suspected stroke.

question

What are the three steps in approaching a coma patient?

answer

1. check for meningitis 2. attempt to reverse by administering thiamine, dextrose and naloxone 3. check brainstem reflexes and focal signs

question

What are the "focal signs?"

answer

hemiparesis aphasia reflex asymmetry facial droop unilateral babinski

question

What are the brainstem reflexes? (5)

answer

*Pupillary*: Shine light into each pupil and look for direct and consensual response. CN 2 in, CN 3 out *Oculocephalic*: Turn head horizontally and vertically and look for conjugate movement in the opposite direction. CN 8 in, CNs 3, 4, 5 out *Caloric*: inject ice water into ear and look for eye deviation towards ear injected. Do if oculocephalic is contraindicated (spine injury) *Corneal*: rub cornea with cotton and look for direct and consensual blink. CN V1 in, CN 7 out *Gag*: gag reflex, 9 in, 10/11 out

question

What are the general causes of depressed consciousness?

answer

Damage to the brainstem, which would cause absent brainstem reflexes Damage to *both* cerebral hemispheres simultaneously Damage to one of the hemispehres with pressure on the other side

question

Structural Causes of depressed consciousness

answer

Focal signs are present. If focal signs are absent, this suggests a diffuse cause, such as metabolic, infectious or toxic *Ischemic stroke* of brainstem or unilateral cerebral hemisphere. *Intracranial hemorrhage*: intraparenchymal, subdural, epidural *Brain Tumor*: with edema or hemorrhage *Brain Abscess*

question

What is the difference between Wernicke's encephalopathy and korsakoff syndrome?

answer

Wernicke's is an acute confusional state brought on by thiamine deficiency in alcoholics Korsakiff is a long-term memory disorder that can arise after Wernicke's has been resolved

question

Vision

answer

p. 26-36

question

What is the approach to weakness?

answer

1. confirm the complaint is indeed weakness and not pain, fatigue, etc 2. identify which muscle(s) are weak 3. Determine the pattern of weakness (muscle, NMJ, nerve, root, plexus, cord, brain) 4. associated symptoms 5. differential 6. labs, imaging

question

Muscles, with their movements, nerves and roots

answer

Table 5-1, p. 40

question

Differential Diagnosis for Peripheral Nerve Disorders

answer

*mononeuropathy*: entrapment (carpel tunnel), systemic vasculitis, metabolic and rheum disease *Polyneuropathy*: demyelinating (charcot marie tooth, GBS), axonal

question

What is the difference between a nerve root and a nerve plexus?

answer

A nerve exits the spinal cord as a *root* and then multiple roots form a *plexus*, in which individual fibers seperate and form peripheral nerves. Peripheral nerves thus often originate in more than one nerve root

question

What is the difference between a neuropathy and a radiculopathy?

answer

neuropathy implies peripheral nerve while radiculopathy implies nerve root

question

Associated signs for neuropathy vs radicupathy

answer

Mononeuropathy: pain Polyneuropathy: sensory loss, loss/diminished reflexes Radiculopathy: radiating tingling, pain, sometimes absent reflexes

question

Muscle Reflexes and their nerve roota

answer

1, 2 buckle my shoe - ankle jerk (S1) 3, 4 kick the door - hip and patellar (L3, L4) 5, 6 pick up sticks - biceps/brachioradialis (C5, C6) 7, 8 lay them straight - triceps, fingers (C7, C8)

question

Radiculopathy differential

answer

single = herniated disc, shingles reactivation poly = inflammatory, infectious

question

How can you tell if an injury is in a peripheral nerve or a plexus?

answer

A plexus injury will manifest as weakness in multiple muscles that have different roots. A peripheral nerve injury will be weakness only in the muscle that nerve supplies

question

Brachia Plexus

answer

MARMU - p. 42

question

Upper Motor Neuron

answer

- Constitutes the neuron from the motor cortex in the cerebral hemisphere through the pyramidal decussation into the spinal cord - Presents as weakness, spasticity, hyperreflexia, positive babinski

question

Lower Motor Neuron

answer

- Constitutes the anterior horn cell and its axon all the way through the root to the NMJ (basically everything outsides the spinal cord) - Presents as wasting and fasciculations

question

Spinothalamic Tract

answer

Lateral: Pain and temperature Anterior: Crude Touch Thinly myelinated or unmyelinated fibers Synapses in the dorsal horn and cross at the level of entry into the cord. Travel *contralaterally* up the cord Then travels up to the ventral posterolateral (*VPL*) nucleus in the thalamus, then to the somatosensory cortex of the postcentral gyrus

question

Dorsal Column

answer

Conscious Proprioception, vibration, well localized touch Heavily myelinated fibers Enter spinal cord and travel *ipsilaterally* up the cord in the nucleus gracilis and cuneatus to the lower medulla, where they cross as the medial lemniscus

question

Spinocerebellar Tract

answer

non conscious proprioception

question

Basic Lesion Localization

answer

*Peripheral Nerve*: sensory loss according to that nerve's territory *Nerve Root*: dermatomal sensory loss *Plexus*: sensory loss in multiple enrve territories *Spinal Cord*: sensory loss below level of lesion *Brainstem*: sensory loss in ipsilateral face and contralateral body *Thalamus/Cortex*: contralateral face, arm, leg

question

Dermatomes

answer

Back of head/neck = C2 Nipple = T4 Umbilucus = T10/T11 Genitals = S2/S3 Upper Leg = L2 Lateral foot = S1 Medial Foot = L5

question

Dissociated Sensory Loss

answer

Loss of a single tract with preservation of other tracts. Ex: Syringomyelia: loss of pain/temp, preservation of proprioception anterior spinal artery stroke: loss of pain/temp, preservation of proprioception Subacute combined degeneration: loss of proprioception, preservation of pain/temp

question

What 4 things could "dizziness" mean?

answer

vertigo: rotational sense of movement lightheadedness: faint-feeling, presyncopal dysequilibrium: imbalance/unsteadyness of legs ill-defined dizziness

question

Peripheral vs central vertigo

answer

Peripheral will have associated tinnitus/hearing loss, nausea, vomiting Central will have associated diplopia, dysarthria, dysphagia, vertical nystagmus

question

causes of vertigo

answer

*vestibular neuronitis*: acute unilateral peripheral vestibulopathy (no inflammation). acute onset, self-resolving *Labyrinthine Concussion*: head injury *Infarct*: (labyrinth, brainstem, cerebellum): PICA and AICA supply the vestibular apparatus and the internal auditory artery is supplied by AICA. sudden onset deafness/vertigo. Will have other neuro deficits *Meniere Disease*: episodic vertigo w/ nausea/vomiting along with fluctuating but progressive hearing loss, tinnitus, sensation of fullness/pressure in ear. Caused by increase in endolymph volume *Perilymph fistula*: the endolymph "pops" during increased pressure (straign) *Benign positional paroxysmal vertigo*: brief attacks of vertigo brought on by positional changes. Caused by free moving calcium carbonate crystals in the semicircular canals

question

Dix Halpike Maneuvar

answer

p. 54 combined vertical/torsional nystagmus treat w/ epley maneuvar (p. 57) t

question

Causes of Syncope

answer

*Neurogenic Syncope*: the pathophysiologic activation of mechanoreceptors leading to cardioinhibition of vasodepression (carried by vagus), leading to hypotension and bradycardia *Autonomic Failure*: failure to release norepi upon standing, leading to inability to vasoconstrict to counteract gravity's pull on blood. Causes could include parkinson's, MSA

question

Friedreich Ataxia

answer

Autosomal recessive progressive ataxia. Affects arms more than legs. Often has severe dysarthria, areflexia, spasticity, impaired vibration and positional sensation. Childhood onset.

question

Inherited Episodic Ataxia

answer

Two types, both marked by brief episodes of ataxia, vertigo, nausea, vomiting EA-1: mutation in voltage gated *potassium* channels. Brief attacks w/ muscle myokymia (quivering) in between attacks EA-2: mutations in pore forming alpha1 subunit in the P/Q type voltage gated *calcium* channels. Attacks are longer (several minutes) with interictal nystagmus

question

Autosomal Domiant Spinocerebellar Degeneration

answer

Insidious (slow) onset of gait and dysarthria n early adulthood. Mild to moderate cognitive decline is a late sign. Some subtypes are due to a *CAG* trinucleotide repeat expansion.

question

Miller Fisher Syndrome

answer

A variant of BGS characterized by the triad of ataxia, areflexia, ophthalmoplegia. The ataxia is due to proprioceptive loss, not cerebellar dysfunction. 90% of patients have IgG-anti-GQ1b antibodies in serum Self-limiting. Full recovery

question

What should you suspect in a patient with ataxia and ophthalmoplegia?

answer

Wernicke's Miller fisher MS cerebellar stroke posterior fossa mass

question

What should you suspect in a patient with ataxia and extrapyramidal signs?

answer

wilson's creutzfeldt jacob olivopontocerebellar atrophy

question

What should you suspect in a patient with ataxia and downbeat nystagmus?

answer

foramen magnum lesion posterior fossa mass

question

Other Gaits

answer

p.61

question

14 yo girl + 3 year history of slowly progressive gait ataxia and slurred speech + nystagmus + absent ankle reflexes + hammering toes + high arched feet + diminished virbatorysense in toes + no family history Diagnosis?

answer

*Friedreich Ataxia* (FRDA), a autosomal recessive mutation in FXN gene on chromosome 9 (GAA repeat of at least 66 units) with damage to cerebellum and peripheral nerves. Onset is between 10 and 15. Diabetes occurs in 30% of FRDA patients Hypertrophic cardiomyopathy occurs in 66% Hearing loss in 13% Patients are fertile

question

What part of the brain controls the bladder? (p. 66)

answer

*Voluntary*: dorsomedial *frontal lobe* ? *medial* pontine micturition center (PMC) ? detrusor muscle contraction ? voiding Lateral PMC ? urethral sphincter contraction ? urine retention *Spinobulbospinal*: bladder ? PMC ? parasympathetic sacral nuclei *Spinal Segmental*: detrusor ? Onuf's nucleus in S2-S4 spinal cord ? striated sphincter muscles (pudendal)

question

What happens when the PMC is damaged?

answer

incontinence? p. 65

question

Urge Incontinence

answer

Involuntary loss of urine along with strong desire to void (i.e. urgency). Detrusor instability (DI). If the cause of the DI is neurologic, it is termed "detrusor hyperreflexia* or spastic bladder. Essentially, the detrusor is contracting too much, reducing bladder capacity and causing involuntary voiding. *Causes*: strokes, frontal lobe dysfunction, suprasacral lesions, MS -> i.e. UMN

question

Detrusor Sphincter Dyssynergia

answer

inappropriate contraction of the external sphincter upon detrusor contraction. This is bad because detrusor contraction forces urine out and sphincter contraction keeps urine in. This usually happens in the context of urge incontinence and can lead to VU reflux and renal damage

question

Stress Incontinence

answer

involuntary loss of urine during periods of increased strain (laughing, sneezing, coughing) due to weakened pelvic floor muscles.

question

Overflow Incontinence

answer

involuntary loss of urine associated with overdistension of the bladder, reflecting a LMN problem. constant dribbling Results in atonic bladder, i.e. ?capacity ?compliance *Causes*: drugs, diabetic neuropathy, lower spinal cord injury, radical pelvic surgery, bladder/urethral obstruction

question

Supraspinal Disease Causing Urinary Incontinence

answer

*Stroke*: hyperreflexic, small bladder with ?urgency and ?frequency. Associated with poor functional outcome *parkinsons*: hyperreflexia, pseudodyssnergia

question

Treatment of Urinary Incontinence

answer

p. 69

question

What nerves are responsible for male sex?

answer

Pudendal: motor and sensory Para S2-S4: erection Sympa - T11-T12:ejaculation

question

What labs are important to get when working up erectile dysfunction?

answer

Prolactin, testosterone, gonadotropins

question

What physical exam findings suggest a physical cause of headache (making the headache secondary to this cause)?

answer

Papilledema = ICP temporal artery tenderness nuchal rigidity - meningitis

question

Migraine

answer

2nd most common headache, after tension Unilateral, throbbing, pulsatile, associated with nausea/vomiting, photophobia, phonophobia Last 3-72 hours May or may not have aura, usually visual (flashing lines, scotoma) Pain is thought to be carried by the trigeminal nucleus caudalis and parasympathetic efferents

question

Tension Headaches

answer

Most common headache Recurrent attacks of bilateral, pressing, squeezing, around the head (vice-like). Not accompanied by nausea or aura, not made worse by physical activity.

question

Cluster Headaches

answer

A rare form of trigeminal autonomic cephalgia (TAC). Unilateral, usually orbital or temporal, trigeminal pain with concurrent ipsilateral autonomic symptoms such as lacrimation, conjuctival injection, facial swelling, eyelid edema, rhinorrea, horner syndrome. All of these, except horner's, occur at the time of headache. Patients like to move around when they get these headaches. Triptans and steroids for aboriton. verapamil, lithium may be helpful for prophylaxis

question

Paroxysmal Hemicrania

answer

Unilateral with autonomic symptoms much shorter than cluster, usually 10-30 minutes more frequent than cluster, up to 40X/day Very responsive to *indomethacin*, an NSAID

question

Subarachnoid headache

answer

"Worst headache of my life" Begins suddenly and peaks in intensity w/in a few seconds of onset = ''thunderclap headache'' Get head CT and LP. Blood or yellow on LP (xanthochromia)

question

Low Pressure Headaches

answer

?Pressure in subarachnoid place or CSF can cause headache. Pain is bilateral. Usually arises as a complication of LP. The "low pressure" is really low volume of CSF, which can be caused by LP or rupture of a CSF pouch/cyst. ?Pain while upright ?Pain while lying down Treatment is recumbency, aggressive fluid replacement, caffeine and, if needed, epidural blood patch

question

Idiopathic Intracranial Hypertension (pseudotumor cerebri)

answer

?Pain while lying down ?Pain while standing upright ?Pain in mornings Accompanied by pulsatile tinnitus and transient visual obstructions, CN 6 palsies, papilledema Can be precipitated by valsalva Typical in young overweight women who often have menstrual abnormalities. Be wary of visual loss (compression of optic nerve) Dx: mass lesion, venous sinus thrombosis Tx: ?ICP via LP, diuretics

question

Temporal Arteritis

answer

giant cell, (women) over 50 claudication inflammatory changes, granulomas

question

chronic daily headache

answer

most likely transformed (chronic) migraine, chronic tension, med overuse or withdrawal

question

Trigeminal Neuralgia

answer

electric shock pain in the trigeminal distribution, often brought on by combing hair, brushing teeth, shaving, eating, drinking, gentle breeze on face may be caused by compression at the cerebellopontine angle. MRI is needed to rule out other compressive lesions Tx: carbamazepine or surgery (percutaneous radiofrequency ablation, microvascular decompression)

question

Postherpetic Neuralgia

answer

pain after shingles. burning, itching, sensitive to touch. pain can remain after rash subsides. TCAs or gabapentin for the pain

question

What are the components of the exam that is used to test aphasias/

answer

Fluency Repetition Comprehension Naming Reading Writing

question

Broca Aphasia

answer

Difficulty producing speech (fluency). Pts have trouble getting the words out and speech has lots of hesitations and false starts. Pts are aware of and frustrated by the aphasia Cannot repeat or write. Can comprehend written instructions Difficulty w/ tricky commands ("under the paper place the pen") *Cause*: superior MCA stroke. Broca's area is in the left (dominant) posterior frontal lobe, bordering the superior temporal lobe *Associated signs*: right sided face/arml weakness

question

Wernicke Aphasia

answer

Impaired comprehension. Cannot understand others and their speech is incomprehensible while speech production is preserved (word salad). Cannot repeat Unaware of their deficit - get angry/paranoid at people *Cause*: damage (stroke) to dominant superior temporal gyrus. Often inferior MCA stroke. *Associated signs*: contralateral (right) homonymous superior quadrantanopia (pie in sky)

question

Conduciton Aphasia

answer

Inability to repeat with preserved fluency and comprehension *Cause*: lesion in arcuate fasciculus, the white matter that connects Broca to Wernicke. Or lesions in temporal/parietal lobes that spares werkicke

question

Transcortical Motor Aphasia

answer

Nonfluent aphasia (i.e. perisulvian broca's) but with preserved repetition. *Cause*: frontal lobe lesion with preservation of the connection between broca and wernicke

question

Transcortical Sensory Aphasia

answer

perisylvian wernicke's but with preserved repetition due to lesion near wernicke *Cause*: left PCA stroke

question

Global Aphasia

answer

wernicke + broca

question

Subcortical Aphasia

answer

lesions in basal ganglia, thalamus weird aphasia

question

Pure Alexia

answer

Patients can write but they cannot read, even what they have just written *Cause*: lesion in dominant occipital lobe and splenium of corpus callosum, interrupting connections between wernicke's and visual cortex.

question

Apraxia

answer

Inability to carry out a task, ex hammer a nail, despite understanding the command and having the motor ability to enact it. It's as if they cannot imagine the execution, despite understanding it *Cause*: dominant frontal lobe = able to recognize the task done by others but cannot do it themselves parietal lesion = cannot recognize it either

question

Agnosia

answer

Inability to recognize objects. could be visual or tactile. due to sensory association lesions

question

Gerstmann's Syndrome

answer

Agraphia + acalculia + right-left confusion + finger agnosia Lesions in dominant inferior parietal lobe (the angular gyrus)

question

Sensory Neglect

answer

Cannot pay attention to left hemisphere, will only draw half a clock. Will also be unable to recognize when a stimulus is applied simultaneously, but will if applied separately. Lesions in nondominant (*right*) frontal or parietal lobe

question

Causes and Dementia and Tests to Run

answer

p. 89

question

Alzheimer's Disease (AD)

answer

usually above 65 yo, more common in women, associated with Down's syndrome and head trauma progressive, beginning with short-term memory impairment

question

AD Genes and Imaging

answer

*ApoE4* and *?2 macroglobulin* on chromosome 19 is a marker for both early and late onset - early onset genes: amyloid precursor protein (*APP*) on chromosome 21, presenilin 1 & 2 (*PS1/2*) on chromosomes 14 and 1 - ?tau ?A?-42 on CSF - hippocampus, amygdala, thalamus greatly reduced in size - bilateral temporoparietal hypometabolism on PET/SPECT scans *Autopsy*: brain atrophy, senile plaque (amyloid deposits) and neurofibrillary tangles (NFTs), which represent phosphorylated tau protein

question

AD Therapy

answer

*Donepezil* (Aricept): Achase inhibitor. SEs include GI and rarely liver *Rivastigmine* (exelon): Achase inhibitor. SEs include GI and rarely liver *Memantine* (namenda): NMDA receptor antagonist. SEs are dizziness, headache, confusion *Galantamine* (razadyne): Achase inhibitor. SEs include GI and weight loss

question

Vascular Dementia

answer

Acute onset/stepwise onset dementia along with focal neuro deficits. Brain imaging shows multiples strokes, lacunes, deep white matter changes. Most patients are hypertensive/diabetic. Must investigate cause of strokes (cardiac, coag).

question

Lewy Body Dementia

answer

The 2nd leading cause of dementia. Marked by cognitive impairment, impaired visuospatial perception and visual memory, fluctuations of alertness, prominent visual hallucinations, delusions, extrapyramidal symptoms, extreme sensitivity to neuroleptics (never give haldol). Death 10-15 years after diagnosis Lewy bodies are eosinophilic intracellular inclusions of ?synuclein. In Parkinson's they are in the substantia nigra In LBD, the *cortical neurons*. Treat with low dose atypical antipsychotics (risperidone, quetiapine)

question

Progressive Supranuclear Palsy (Steele-Richardson-Olszewski Syndrome)

answer

Failure of vertical gaze, dysarthia, dysphagia, extrapyramidal rigidity, gait ataxia, apathy and dementia. Atrophy of dorsal midbrain, globus pallidus, subthalamic nucleus Subcortical NFTs, neuron loss, gliosis Median survival = 6-10 years

question

Huntington Disease

answer

Autosomal dominant CAG repeat on chromosome 4. Requires at least 40 repeats for symptoms Onset 35-45 yo. Triad of chorea, behavior/personality changes (OCD, aggression) and dementia. Destruction of caudate/putamen (striatal GABA-nergic neurons) and loss of cortical neurons. The mutation causes flawed processing of proteins, resulting in deposits in nuclei and activation of cell death Treatment is dopamine antagonists

question

Frontotemporal Lobar Dementia

answer

First signs are congitive/behavioral, not memory.

question

Prion Disease

answer

Spongy degeneration, neuronal loss, gliosis, astrocytic proliferation CJD: rapidly progressive dementia, pyramidal signs, myoclonus, sharp waves on EEG. CSF is normal but may have 14-3-3 protein

question

HIV Associated Dementia

answer

HIV can cause encephalitis and also make patients prone tpo other CNS infections (toxo, TB, syphilis)

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