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USMLE Step 2 > neuroscience > Flashcards

neuroscience Flashcards

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USMLE® Step 1 flashcards
1
Q

Neurofibromatosis type 1 (NF1)

A
  • neurocutaneous syndrome characterized by cafe-au-lait macules and tumors of the skin and central and peripheral nervous systems
  • an MRI of the brain and orbits is the best modality for a detailed evaluation of soft-tissue anatomy in any NF1 patient w/ concerning neurologic symptoms (eg, chronic headache, vision changes, early-morning vomiting)
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2
Q

Bilateral acoustic neuromas (vestibular schwannomas) can cause sensorineural hearing loss and are diagnostic of neurofibromatosis type 2. AUDIOMETRY is the best initial screening lab test for the diagnosis of acoustic neuromas, but its not indicated for NF1.

A

.

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3
Q

main clinical features of Neurofibromatosis type 1

A
  • cafe-au-lait spots
  • multiple neurofibromas
  • lisch nodules
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4
Q

main clinical features of neurofibromatosis type 2

A

bilateral acoustic neuromas

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5
Q

Tuberous sclerosis

A
  • neurocutaneous genetic (TSC1 and TSC2 genes) syndrome associated w/ intracranial tumors (eg, cortical tubers or hamartomas, subependymal giant cell astrocytomas, subependymal nodules).
  • other characteristics: hypopigmented macules (ash leaf spots), facial angiofibromas, cardiac rhabdomyomas, renal angioleiomyomas, mental retardation, and seizures
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6
Q

suspect multiple sclerosis in a patient with neurological deficits that cannot be explained by a single lesion. Exacerabation of these neurological deficits by hot weather or exercise are a useful clue.

A

.

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7
Q

Internuclear ophthalmoplegia is a characteristic finding of what?

A

Multiple sclerosis

-due to demyelination of the medial longitudinal fasciculus in the dorsal pontine tegument

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8
Q

lesion of the optic nerve

A

blindness in the same eye

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9
Q

lesion of the optic chiasm

A

-bitemporal hemianopia

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10
Q

lesion of the optic radiation

A

contralateral hemianopia

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11
Q

lesion of the oculomotor nerve

A

-ptosis and the eye looking down and out, due to unopposed actions of the lateral rectus and superior oblique muscles

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12
Q

lesion of the trochlear nerve

A

vertical diplopia and extorsion of eye

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13
Q

lesion of the abducens nerve

A

convergent strabismus and horizontal diplopia

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14
Q

lesion of the medial lemniscus

A

affects touch and vibration sensations bilterally

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15
Q

destruction of the frontal eye field in frontal lobe

A

ipsilateral deviation of the eyes

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16
Q

Huntington’s disease

A
  • suspect in a patient w/ mood disturbances, dementia, chorea and a family hx of similar symptoms
  • autosomal dominant and affects both sexes equally
  • age at presentation is typically between 30-50 years
  • facial grimacing, ataxia, dystonia, tongue protrusion, writhing movements of extremities
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17
Q

pseudodementia

A

-severe depression in the elderly which presents with a dementia similar to alzheimer’s disorder

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18
Q

Pick’s disease

A
  • similar in presentation to Alzheimer’s disease, except that it presents at an earlier age
  • seen more frequently in females, and frequently causes personality changes due to involvement of the frontal lobes
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19
Q

Carpal tunnel syndrome

A
  • most common mononeuropathy of the upper extremity; paresthesias of the first three-and-a-half digits and occasionally the thenar eminence atrophy are typical
  • carpal tunnel is a fibro-osseous structure formed by the carpal bones and covered by the transverse carpal ligaments; median nerve passes through this tunnel along w/ the tendons of FLEXOR DIGITORUM SUPERFICIALIS, FLEXOR DIGITORUM PROFUNDUS, and FLEXOR POLLICIS LONGUS
  • it develops in 7% of pts w/ hypothyroidism
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20
Q

location where entrapment of the median nerve can occur

A
  • carpal tunnel is most common
  • also in the forearm during pronator teres syndrome
  • also at the elbow; deep flexors of the digits are involved, but cutaneous sensation is usually spared
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21
Q

alzheimer disease

A
  • early, insidious short-term memory loss
  • language deficits and spatial disorientation
  • later personality changes
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22
Q

vascular dementia

A
  • STEPWISE decline
  • early executive dysfunction
  • CEREBRAL INFARCTION and/or deep white matter changes on neuroimaging
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23
Q

Frontotemporal dementia

A
  • EARLY PERSONALITY CHANGES
  • apathy, disinhibition and compulsive behavior
  • FRONTOTEMPORAL ATROPHY on neuroimaging
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24
Q

Lewy body dementia

A
  • VISUAL HALLUCINATIONS
  • spontaneous PARKINSONISM (rigidity, bradykinesia, gait disturbance)
  • fluctuating cognition
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25
Q

normal pressure hydrocephalus

A
  • ATAXIA early in disease
  • urinary INCONTINENCE
  • DILATED VENTRICLES on neuroimaging
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26
Q

Prion disease

A
  • behavioral changes
  • RAPIDLY PROGRESSIVE
  • MYOCLONUS and/or seizures
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27
Q

Mild cognitive impairment

A
  • considered an intermediate stage between normal aging and dementia (from any etiology) and is associated w/ an increased risk for developing dementia
  • it should NOT interfere w/ social or occupational function
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28
Q

Normal aging

A

-associated w/ a gradual decline in mental processing capacity and can result in occasional forgetfulness but should not interfere w/ activities of daily living

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29
Q

vascular dementia

A
  • presents as a sudden or stepwise decline in executive function after stroke, which interferes w/ activities of daily living
  • pts typically have abnormal neurologic findings on exam
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30
Q

Migraine headaches in peds

A
  • migraines are the most common cause of acute and recurrent headaches in the pediatric population (occur before age 20 in 50% of cases)
  • typically present w/ unilateral or bifrontal pain, photophobia, phonophobia, nausea, vomiting, and a visual, auditory, or linguistic aura
  • first line tx in children includes acetaminophen, NSAIDs, and supportive care; Triptans may be tried if these measure are not effective
  • although migraines in kids may be bifrontal, occipital headaches are extremely rare, and if present should raise concern for a structural lesion
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31
Q

The vast majority of pts who present w/ migraine symptoms in the context of a normal neurologic exam do NOT require neuroimaging. what are the indication of neuroimaging in kids w/ a headache?

A

-hx of coordination difficulties, numbness, tingling, focal neurologic signs, hx of headache that causes awakening from sleep, hx of increasing headache frequency

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32
Q

most appropriate next step in management for patient who presents w/ pseudotumor cerebri (idiopathic intracranial hypertension)?

A

lumbar puncture

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33
Q

indications for ophthalmology referral in corneal trauma

A

-ulceration, pus, drop in visual acuity, lack of healing within 3-4 days

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34
Q

common causes of trigeminal nerve dysfunction

A

-tumor, trauma, prior herpes zoster infection

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35
Q

corneal abrasion

A
  • trauma, foreign body lodging under the lid, and contact lens use leading to corneal epithelial defect
  • abrasion can also occur w/o obvious corneal trauma
  • pts typically develop severe eye pain, photophobia w/ reluctance to open the eye, and a sensation of a foreign body in the eye
  • absence of eye pain suggests trigeminal nerve dysfunction as the ophthalmic branch (V1) of the trigeminal nerve (cranial nerve V) controls corneal sensation
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36
Q

facial nerve (CN VII)

A
  • facial movement, taste in the anterior 2/3 of the tongue, lacrimation (via the greater petrosal/vidian nerves), salivation (via chorda tympani), and eyelid closure
  • also carries sensory fibers supplying sensation to parts of the external ear and the nasopharynx
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37
Q

oculomotor nerve (CN III)

A
  • majority of eye movement (adduction via the medial rectus, elevation via the superior rectus and inferior oblique, and depression via the inferior rectus), eyelid opening, and pupillary constriction
  • its a pure motor nerve carrying general somatic efferent and general visceral efferent fibers
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38
Q

optic nerve (CN II)

A
  • carries visual info to the brain as well as mediates the afferent limb of the pupillary light reflex pathway
  • damage to this nerve can cause monocular blindness and an afferent pupillary defect; however, corneal sensation would be spared
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39
Q

vagus nerve (CN X)

A
  • responsible for swallowing, palate elevation, phonation, and parasympathetic outflow to the thoracoabdominal viscera, including monitoring of the aortic arch baro- and chemoreceptors
  • the vagus nerve is also responsible for taste in the epiglottis and sensation from parts of the external ear; also mediates the afferent limb of the cough reflex and the efferent limb of the gag reflex
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40
Q

Multiple system atrophy (Shy-Drager syndrome)

A
  • degenerative disease characterized by the following:
  • parkinsonism
  • autonomic dysfunction (postural hypotension, abnormal sweating, disturbance of bowel or bladder control, abnormal salivation or lacrimation, impotence, gastroparesis, etc.)
  • widespread neurological signs (cerebellar, pyramidal or lower motor neuron)
  • the accompanying bulbar dysfunction and laryngeal stridor may be fatal
  • anti-parkinsonism drugs are generally ineffective, and tx is aimed at intravascular volume expansion w/ fludrocortisone, salt supplementation, alpha-adrenergic agonists, and application of constrictive garments to the lower body
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41
Q

always consider what when a pt w/ Parkinsonism experiences orthostatic hypotension, impotence, incontinence, or other autonomic symptoms?

A

-Multiple system atrophy (Shy-Drager syndrome)

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42
Q

Idiopathic orthostatic hypotension

A

-seen secondary to the degeneration of postganglionic sympathetic neurons; pathology is confined to the autonomic nervous system

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43
Q

Horner’s sydnrome

A

-regional dysautonomia characterized by ANHIDROSIS, MIOSIS, and PTOSIS

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44
Q

Riley-Day syndrome (familial dysautonomia)

A
  • autosomal recessive disease seen predominantly in children of Ashkenazi Jewish ancentry
  • characterized by gross dysfunction of the autonomic nervous system w/ severe orthostatic hypotension
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45
Q

Absence (petit mal) seizures

A
  • characterized by sudden cessation of mental activity
  • an episode is very short, but may occur repeatedly throughout the day
  • there are NO associated complex automatisms or tonic-clonic activity
  • the diagnosis is best confirmed by EEG studies (activation procedures such as hyperventilation, photic stimulation, sleep helps further in diagnosis)
  • NO postictal somnolence or confusion
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46
Q

EMG studies

A
  • used to diagnose PERIPHERAL nerve disorders
  • EMG is used to analyze the neuromuscular system, differentiate disease of neuromuscular system from primary neuropathies
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47
Q

side effects of anabolic steroids

A

-increased aggression, acne, baldness, gynecomastia, hepatic dysfunction, altered lipid profiles, virilization, testicular failure, and mood and behavior changes

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48
Q

Petit mal seizures

A
  • characterized by a sudden cessation of mental activity
  • an episode is very short, but may ocur repeatedly throughout the day
  • there are no associated complex automatisms or tonic-clonic activity
  • diagnosis is best confirmed by EEG studies
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49
Q

Brown-Sequard syndrome

A

-associated w/ damage to the lateral spinothalamic tracts, causing contralateral loss of pain and temperature sensation beginning TWO LEVELS BELOW THE LEVEL OF THE LESION

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50
Q

Damage to the lateral spinothalamic tracts (pain and temp) causes contralateral loss of pain and temp sensation beginning 2 levels BELOW the level of the lesion.

A

.

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51
Q

In elderly pts w/ multiple medications, it is very important to regularly assess their general well-being and current medication list, as well as to promote patient adherence to the appropriate regimen. Hemorrhages are seen as HYPERDENSE areas on CT scan, while infarcts characteristically have HYPODENSE parenchymal areas on CT scan.

A

.

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52
Q

Subarachnoid hemorrhage

A
  • sudden onset of severe headache
  • lethargy, coma, or vomiting
  • non-contrast CT is diagnostic study of choice, and shows blood in the sulci and cisternae
  • in 10% of pts, the CT scan is normal, and lumbar puncture is required to confirm the diagnosis
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53
Q

what do infarcts look like on CT scan?

A

-HYPODENSE parenchymal areas on CT

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54
Q

Lacunar infarcts

A

-usually present with pure motor stroke, pure sensory stroke, or clumsy-hand dysarthria

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55
Q

Cerebellar hemorrhage

A
  • may include inability to walk, occipital headache, neck stiffness, gaze palsy, and facial weakness
  • CT scan would reveal HYPERDENSE area
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56
Q

Staging of pressure ulcers

A

Stage 1: nonblanchable redness w/ intact skin
Stage 2: shallow open ulcer w/ a partial thickness loss of dermis
Stage 3: possible visualization of subcutaneous fat w/ a full thickness tissue loss
Stage 4: exposed bone, tendon or muscle w/ possible slough or eschar

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57
Q

Diabetic foot ulcers

A
  • result from chronic unnoticed trauma due to advanced peripheral neuropathy and poor wound healing from microvascular insufficiency
  • its believed that peripheral neuropathy plays a bigger role in pathogenesis
  • these wounds occur most commonly on the soles of the feet over the metatarsal heads and the top of the toes w/ Charcot deformity
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58
Q

Venous stasis ulcers

A
  • occur in the setting of chronic lower extremity edema and occur on the pretibial area of the lower leg or above the medial malleolus in the ankle
  • they often begin insidiously on a background of stasis dermatitis
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59
Q

arterial ulcers

A
  • due to arterial occlusive disease that blocks blood supply and causes tissue necrosis
  • they usually occur in the most distal parts of the body where blood supply is lowest such as tip of the toes
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60
Q

continued pressure on a bony prominence for a prolonged period of time can result in ischemic necrosis of overlying muscle, subcutaneous tissue, and skin leading to formation of a pressure (decubitus) ulcer. Caregivers should reposition vulnerable pts regularly to reduce the incidence of decubitus ulcers

A

.

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61
Q

Most concerning complications of subarachnoid hemorrhage?

A
  • REBLEEDING is the major cause of death within the FIRST 24 HOURS or presentations, especially within the first 6 hours of untreated SAH
  • VASOSPASM can occur in up to 30% of SAH pts from DAYS 3-10 after presentation and is the major cause of delayed morbidity and death
  • CT ANGIOGRAPHY is preferred for detecting vasospasm, which can best be prevented w/ initiation of NIMODIPINE
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62
Q

Hemiplegic migraine

A
  • rare familial disorder that presents w/ migraine headache associated w/ unilateral motor deficits
  • the neurological deficits usually occur at the time of the headache instead of days later
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63
Q

Todd’s palsy

A

-usually occurs after a focal motor seizure

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64
Q

subacute hydrocephalus following subarachnoid hemorrhage

A
  • can present w/ headaches
  • pts tend to develop progressive mental decline and multiple neurologic deficits due to compression of the cranial nerves, brainstem, and/or cerebral cortex
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65
Q

Vasospasm is the major cause of delayed morbidity and mortality in subarachnoid hemorrhage and can result in cerebral infarction. Vasospasm can best be prevented w/ initiation of what?

A

NIMODIPINE

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66
Q

Primidone

A
  • an anticonvulsant agent that converts to phenylethylmalonamide and phenobarbital, which can be used to treat benign essential tremors (along w/ beta-blockers)
  • its administration can precipitate acute intermittent porphyria, which can be diagnosed by checking for urine porphobilinogen
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67
Q

Alcohol is sometimes given to treat benign essential tremors, but it is not routine.

A

.

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68
Q

first-line tx for essential tremors?

A

beta-blockers (not recommended if patient is bradycardic or has severe COPD)

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69
Q

Amyotrophic lateral sclerosis (ALS)

A

-characterized by the presence of both upper (spasticity, bulbar symptoms, hyperreflexia) and lower (fasciculations) motor neuron lesions

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70
Q

A degree of memory impairment is common as people age. While memory impairment is more severe in pts w/ dementia versus normal changes of aging, the key distinction is what?

A
  • Pts w/ dementia have impaired functioning due to their poor memory
  • impairment of daily functioning is essential in distinguishing between dementia and normal changes of aging.
  • pts w/ dementia have functional impairments
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71
Q

Migraine

A
  • should be suspected in pts w/ a unilateral headache w/ a pulsatile quality, particularly if it is accompanied by vomiting and photophobia
  • IV antiemetics (chlorpromazine, prochlorperazine, or metoclopramide) can be used as monotherapy for acute migraine attacks, particularly in pts w/ accompanying nausea and vomiting
  • amitriptyline and propranolol are effective PROPHYLACTIC medications, but not helpful in acute setting
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72
Q

when should you suspect neurofibromatosis type II?

A
  • in a young patient w/ acoustic neuroma and multiple cafe-au-lait spots
  • MRI w/ gadolinium enhancement is the best method to diagnose acoustic neuromas
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73
Q

Cluster headache

A
  • usually presents w/ acute, severe retroorbital pain that wakes the patient from sleep, peaks rapidly, and lasts for approx. 2 hours
  • more common in men
  • may be accompanied by redness of the ipsilateral eye, tearing, stuffed or runny nose, and ipsilateral Horner’s syndrome
  • attacks occur in clusters, daily, for 6-8 wks, followed by remission lasting up to a year
  • prophylaxis is key!! (verapamil, lithium, and ergotamine)
  • for ACUTE ATTACKS: inhalation of 100% oxygen and subcutaneous sumatriptan
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74
Q

Multiple sclerosis (MS)

A
  • autoimmune inflammatory demyelinating disease of the CNS affecting primarily women of child-bearing age
  • acute exacerbations should be tx w/ high dose IV glucocorticoids
  • Plasma exchange is reserved for pts who do not respond to high dose steroids
  • optic neuritis, Lhermitte’s sign, internuclear ophthalmoplegia, fatigue, Uhthoff’s phenomenon (heat sensitivity), sensory symptoms (paresthesia, numbness), motor symptoms (paraparesis, spasticity), bowel/bladder dysfunction
  • diagnoses by clinical or imaging findings disseminated in time and space (periventricular, juxtacortical, infratentorial, or spinal cord)
  • Oligoclonal IgG bands on CSF analysis
  • relapsing-remitting (majority), primary progressive, secondary progressive, progressive relapsing
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75
Q

subdural hematoma

A
  • results from rupture of bridging veins
  • EPIDURAL hematoma results from rupture of middle meningeal artery
  • semi-lenticular hematoma on CT
  • more common in elderly and alcoholics due to brain atrophy and possible use of anticoagulation therapy
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76
Q

epidural hematoma

A
  • rupture of middle meningeal artery from trauma to temporal bone
  • biconvex hematoma on CT
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77
Q

intracerebral hemorrhage

A
  • results from hypertensive hemorrhage usually

- most common sites are the PUTAMEN and THALAMUS

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78
Q

subarachnoid hemorrhage

A

-rupture of an aneurysm and sometimes head trauma

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79
Q

tumor in the arachnoid granulation

A

meningoma

-usually seen over the convex surfaces of the brain

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80
Q

Argatroban

A
  • direct thrombin inhibitor that reversibly binds to the active thrombin site of free and clot-associated thrombin
  • used mainly for prophylaxis or treatment of thrombosis in pts w/ heparin-induced thrombocytopenia
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81
Q

agents used for primary or secondary prevention of ischemic stroke

A

antiplatelet agents (aspirin, clopidogrel) and statins

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82
Q

IV tissue plasminogen activator (alteplase) is typically useful in acute ischemic stroke within 3-4.5 hours of symptom onset

A

.

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83
Q

vitamin B12 deficiency

A
  • paresthesias and ataxia associated with loss of vibration and position sense
  • severe weakness, spasticity, clonus, and paraplegia, memory loss or cognitive impairment
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84
Q

Tick-borne paralysis

A
  • characterized by rapidly progressive ascending paralysis (which may be asymmetrical), absence of fever and sensory abnormalities, and normal CSF exam
  • Ticks must feed for 4-7 days before they release the neurotoxin, and are typically found on pts after meticulous searching
  • removal of the tick results in spontaneous improvement in most pts
  • NO autonomic dysfunction (unlike that seen in majority of pts w/ Guillain-Barre syndrome)
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85
Q

Guillain-Barre Syndrome (GBS)

A
  • presents w/ an ascending symmetrical paralysis over days to weeks, but not usually hours
  • sensation is usually normal to mildly abnormal
  • autonomic dysfunction (eg. tachycardia, urinary retention, and arrhythmias) occurs in 70% of pts
  • the CSF exam typically is abnormal and may show ALBUMINOCYTOLOGIC dissociation (high protein with few cells). This finding may not be present early in the course, but is present in 80-90% of pts at 1 week
  • Tx: IVIG or plasmapharesis
  • Can be difficult to differentiate from tick-borne paralysis in some cases; however, meticulous search for a tick is very easy to perform
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86
Q

Botulism

A
  • DESCENDING paralysis and early CRANIAL NERVE involvement

- Pupillary abnormalities are common

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87
Q

Spinal cord tumors

A
  • may present w/ ascending paralysis over days to weeks
  • sensation is either mildly or grossly abnormal
  • MRI confirms; tx is IV steroids (methylprednisone)
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88
Q

pts w/ a suspected stroke

A
  • must order immediate non-contrast head CT
  • this is a critical branchpoint in management; pts w/ ischemic stroke are candidates for thrombolytic therapy possibly, while those w/ hemorrhagic stroke are not
  • CT can immediately visualize hemorrhagic strokes, but ischemic strokes might not be visible untile >24 hours after the event
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89
Q

Todd’s paralysis

A

-focal neurologic deficit following a seizure

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90
Q

what are used to diagnose peripheral neuropathy?

A

nerve conduction studies

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91
Q

when suspicion for subarachnoid hemorrhage is high but head CT is negative, what is the next step in management?

A

Lumbar puncture (xanthochromia on exam)

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92
Q

Carotid dopplers are often performed in pts w/ suspected ischemic stroke to identify carotid artery plaques, a common cause of unilateral embolic strokes

A

.

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93
Q

Echocardiography can be an important component of the work-up of suspected ischemic stroke, to identify potential cardiac sources of emboli

A

.

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94
Q

Lacunar strokes

A
  • 25% of ischemic strokes
  • due to microatheroma and LIPOHYALINOSIS in small penetrating arteries of the brain
  • they often affect the INTERNAL CAPSULE (especially the posterior limb) and result in pure motor dysfunction
  • HTN, HLD, smoking, and DM are major risk factors
  • usually of THROMBOTIC origin
  • pts have symptoms affecting the CONTRALATERAL face, arm, and leg EQUALLY
  • other common lacunar stroke syndromes are ataxic hemiparesis, clumsy-hand dysarthria, pure sensory stroke, and mixed sensory-motor stroke
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95
Q

symptoms of elevated intracranial pressure?

A

-headache, vision changes, nausea, vomiting, papilledema

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96
Q

cocaine and methamphetamines can cause strokes due to drug-induced vascular spasm.

A

.

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97
Q

migraine presentation

A

-UNILATERAL, throbbing pain, nausea, phonphobia, photophobia

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98
Q

glucocorticoid-induced myopathy

A
  • progressive proximal muscle WEAKNESS and atrophy WITHOUT PAIN or tenderness
  • lower-extremity muscles are more involved
  • ESR and CK are NORMAL
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99
Q

Polymyalgia rheumatica

A
  • muscle PAIN AND STIFFNESS in the shoulder and pelvic girdle
  • tenderness w/ decreased ROM at shoulder, neck and hip
  • RESPONDS rapidly to GLUCOCORTICOIDS
  • ESR is INCREASED; CK is normal
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100
Q

Inflammatory myopathies

A
  • muscle pain, tenderness, and proximal muscle weakness
  • SKIN RASH and INFLAMMATORY ARTHRITIS may be present
  • ESR and CK are INCREASED
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101
Q

Statin-induced myopathy

A
  • prominent muscle pain/tenderness with or without weakness
  • rare rhabdomyolysis
  • ESR is normal; CK is INCREASED
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102
Q

Hypothyroid myopathy

A
  • muscle pain, cramps and weakness involving the proximal muscles
  • delayed tendon reflexes and myoedema
  • occasional rhabdomyolysis
  • features or hypothyroidism are present
  • ESR is normal; CK is INCREASED
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103
Q

Glucocorticoid-induced myopathy

A
  • complication of chronic corticosteroid use
  • characterized by painless proximal muscle weakness, which is more prominent in the lower extremities
  • there is no muscle inflammation or tenderness, and creatine kinase level and ESR are normal
  • it slowly improves once the offending med is d/c
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104
Q

mononeuritis multiplex

A
  • usually seen in vasculitis and is caused by nerve damage in 2 or more nerves in separate parts of the body
  • pts typically develop asymmetric peripheral nerve findings such as wrist or foot drop
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105
Q

neuromuscular junction disease

A
  • eg myasthenia gravis
  • may cause proximal muscle weakness
  • upper more than lower extremity disease and usually have ocular symptoms
  • fluctuating; more muscle weakness is observed later in the day and following exercise
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106
Q

Polymyalgia rheumatica

A
  • can be seen in up to 50% of pts w/ temporal arteritis!!!!
  • pts typically complain of aching and morning stiffness, w/ pain and decreased ROM in the shoulders, neck, and hip girdle
  • pts have objectively NORMAL MUSCLE STRENGTH
  • the ESR is usually elevated > 40 mm/hr
  • SYMPTOMS IMPROVE RAPIDLY (IN DAYS) W/ GLUCOCORTICOIDS, and ESR usually returns to normal in a few weeks
  • CK is normal
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107
Q

which med may slow the long-term progression of MS?

A

INTERFERON-BETA
-several well-designed clinical trials have proven that IF-beta decreases the frequency of relapse, and reduces disability in pts w/ the relapsing-remitting form of MS

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108
Q

heat stroke

A
  • exertional and non-exertional
  • exertional heat STROKE occurs in otherwise healthy individuals undergoing conditioning in extreme heat and humidity due to thermoregulation failure
  • heat EXHAUSTION is due to inadequate fluid and salt replacement
  • CNS dysfunction (altered mental status) is NOT present in heat EXHAUSTION
  • know the difference between heat stroke and heat exhaustion!
  • heat stroke: temp > 40C (105F), altered mental status, hypotension, tachycardia, tachypnea; may have moist or dry skin and often are NOT volume-depleted; rhabdomyolysis and organ damage can occur above 105F.
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109
Q

pathophysiology of fever

A
  • cytokine activation during inflammation

- temp are usually

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110
Q

pathophysiology of malignant hyperthermia

A
  • uncontrolled efflux of calcium from the sarcoplasmic reticulum
  • rare autosomal dominant disorder
  • occurs in genetically susceptible pts after administration of the anesthetic drugs halothane and succinylcholine and may be associated w/ severe hyperthermia (up to 113F)!
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111
Q

Heat exhaustion

A
  • different than heat stroke!
  • due to inadequate sodium and water replacement during physical activity; due to body’s inability to maintain adequate cardiac output
  • core body temp is usually
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112
Q

Hypertrophic cardiomyopathy

A
  • results in cardiac outlet obstruction
  • like exertional heat stroke, it often occurs in young, physically active individuals
  • symptoms: dyspnea, palpitations, syncope, and sudden cardiac death
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113
Q

Myasthenia crisis

A
  • life-threatening condition characterized by diplopia, ptosis, weakness of the proximal muscles, and weakness of the bulbar muscles and diaphragm leading to respiratory distress
  • pts w/ declining respiratory status (declining oxygen sat, vital capacity, max inspiratory force) should be intubated for airway protection (AChE inhibitors are usually stopped to reduce secretions)
  • Tx: corticosteroids PLUS IVIG or plasmapheresis
  • infection is the most common underlying precipitant and should be treated appropriately
  • differentiated myasthenic crisis from MG cholinergic crisis by the Edrophonium test (short acting AChE; pts get better if myasthenic crisis and worse if MG cholinergic crisis)
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114
Q

Atropine

A

-anticholinergic agent that may be used to prevent the muscarinic side effects of AChE therapy in pts w/ myasthenia gravis

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115
Q

Oral corticosteroids are generally used to treat moderate Myasthenia Gravis symptoms. Approx. 1/3 of pts started on oral corticosteroids can have worsening symptoms. For this reason, the dose is usually titrated very slowly in outpatient setting. However, methylprednisone is preferred in combo w/ plasma exchange in the setting of severe myasthenic symptoms w/ respiratory distress.

A

.

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116
Q

Restless legs syndrome

A
  • urge to move the legs and is accompanied by dysesthesias that are worsened by inactivity and improved w/ movement
  • symptoms are worse in the evening/night
  • Tx: iron supplementation for iron deficiency, conservative measures (leg massage, heating pad, exercise, avoiding sleep deprivation), and pharmacotherapy w/ dopamine agonists (pramipexole, ropinirole) or alpha-2-delta calcium channel ligands (eg. gabapentin)
  • can be idiopathic or secondary to iron deficiency anemia, pregnancy, uremia, diabetes mellitus, Parkinson disease, MS, or meds (antidepressants, metoclopramide)
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117
Q

Acetylcholine

A

-principal neurotransmitter in the PNS; also involved in CNS and autonomic systems

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118
Q

Benzodiazepines

A

-bind to GABA receptors and enhance the inhibitory effect of GABA (increases frequency of opening of receptors)

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119
Q

Serotonin

A
  • neurotransmitter involved in CNS and gastrointestinal signaling processes
  • decreased in depression and anxiety
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120
Q

Syringomyelia

A
  • fluid-filled cavity located within the cervical and thoracic spinal cord that is most commonly associated w/ Arnold Chiari malformation type 1
  • pts typically present w/ areflexia weakness in the upper extremities and dissociated sensory loss following a “cape” distribution
  • dilation of central canal or a separate cavity within the spinal parenchyma
  • loss of pain/temp sensation in the dermatomes corresponding to site of spinal involvement, but vibration/proprioception is preserved
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121
Q

vitamin B12 deficiency

A
  • can cause degeneration of the dorsal and lateral spinal tracts (subacute combined degeneration)
  • typically presents w/ impaired vibration/proprioception and spastic muscle weakness
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122
Q

Anterior spinal cord syndrome

A
  • presents w/ sudden flaccid paralysis (spinal shock) and loss of pain/temperature sensation below the level of spinal injury
  • autonomic dysfunction may also occur due to interruption of descending autonomic tracts
  • risk factors: aortic surgery or dissection
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123
Q

transverse myelitis

A
  • segmental demyelination/inflammation of the spinal cord
  • may occur w/ MS
  • subacute onset of flaccid paralysis (spinal shock) and loss of all types of sensation below the level of spinal injury
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124
Q

Cervical spondylotic myelopathy

A

-may present in older adults w/ progressive neck pain, and various symptoms/sign of radiculopathy and myelopathy

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125
Q

typical CT/MRI findings in high-grade astrocytoma?

A

-heterogenous and serpiginous contrast enhancement

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126
Q

typical CT/MRI findings in glioblastoma multiforme (GBM)?

A

-butterfly appearance w/ central necrosis

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127
Q

brain abscess

A
  • high fever, acute onset, evidence of systemic infectious process
  • uniform contrast enhancement
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128
Q

brain metastasis

A
  • usually have a duration of symptoms of less than 2 months
  • site of metastasis is the gray-white junction or watershed zones
  • usually multifocal and spherical in shape
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129
Q

low-grade astrocytoma

A
  • seizures, longer duration of symptoms

- contrast enhancement is less likely

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130
Q

the most common site of ulnar nerve entrapment

A

-at the ELBOW where the ulnar nerve lies at the medial epicondylar groove

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131
Q

Vitamin B12 deficiency

A
  • can result from chronic malabsorption (Crohn disease, ileal resection, chronic atrophic gastritis, gastrectomy) and manifest clinically as macrocytic anemia and subacute combined degeneration. Peripheral blood smear: Macro-ovalocytes and hypersegmented neutrophils
  • numbness/paresthesias, imparied proprioception/vibration sense, gait ataxia, UMN signs such as spastic weakness and hyperreflexia, peripheral neuropathy, memory loss, dementia
  • serum methylmalonic acid (MMA) levels should be obtained in pts w/ borderline B12 levels as elevations in MMA are more sensitive in detecting vitamin B12 deficiency than serum vitamin levels alone
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132
Q

D-lactic acidosis

A
  • rare condition that can occur in pts w/ short-bowel syndrome
  • unabsorbed carbs are metabolized by intestinal bacteria that produce D-lactic acid, which becomes systemically absorbed
  • usually asymptomatic but can develop episodes of confusion, ataxia, and dysarthria during carb loading
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133
Q

AL amyloidosis

A

-monoclonal gammopathy and multiple myeloma can cause this
-presents w/ polyneuropathy and anemia
-

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134
Q

hypothyroidism

A
  • can cause macrocytic anemia and polyneuropathy

- neuro exam shows reduction in deep-tendon reflexes and a delayed relaxation phase

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135
Q

what should you suspect in an HIV-infected patient w/ an altered mental status, EBV DNA in the CSF, and a solitary, weakly ring-enhancing periventricular mass on MRI?

A

Primary CNS lymphoma

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136
Q

Toxoplasmosis

A
  • MRI usually shows multiple, ring-enhancing, spherical lesions in the basal ganglia
  • a positive toxoplasma serology is quite common in normal subjects in the US and is therefore NOT specific for toxoplasmosis (the disease)
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137
Q

Progressive multifocal leukoencephalopathy lesions are NON-enhancing, and do not produce mass effects.

A

.

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138
Q

AIDS dementia complex

A

-imaging reveal cortical and subcortical atrophy and secondary ventricular enlargement

139
Q

Trigeminal neuralgia

A
  • pain in the distribution of CN V
  • clinical diagnosis based on pain, which is severe, intense, burning or electric shock-like
  • paroxysmal that last a few seconds to minutes each, but occurs many times a day
  • Carbamazepine is the drug of choice
140
Q

Burning mouth syndrome

A
  • rare cause of facial pain, caused by a virus and the individual has reddened mucosa and significant pain
  • condition is aggravated by dryness
  • tx is supportive care
141
Q

Medications that block the dopamine (D2) receptor (eg. typical antipsychotics, some atypical antipsychotics, metoclopramide) may cause extrapyramidal effects. Drug-induced parkinsonism typically presents w/ bradykinesia, rigidity, and tremor.

A

.

142
Q

Acute dystonia

A
  • sudden onset of sustained muscle contractions resulting in twisting and abnormal postures (eg torticollis)
  • tx: benztropine or diphenhydramine
143
Q

akathisia

A
  • subjective, restlessness, inability to sit still

- tx: benzodiazepine (lorazepam)

144
Q

tardive dyskinesia

A
  • gradual onset after > 1-6 months of therapy
  • dyskinesia of the mouth, face, extremities
  • no effective tx
145
Q

benign essential tremor

A
  • action tremor that worsens w/ fine motor activity

- typically the only abnormal neuro finding

146
Q

dementia w/ Lewy bodies

A

-older adults w/ fluctuating cognition, parkinsonism, and visual hallucinations

147
Q

Torticollis

A
  • common form of focal dystonia involving the sternocleidomastoid muscle
  • can occur idiopathically, but is very often medication-related (typical antipsychotics, metoclopramide, and prochlorperazine)
  • discontinuation of causative agent may improve symptoms
148
Q

Parkinson’s disease

A

-resting tremors, bradykinesia, rigidity, postural instability

149
Q

Essential tremor

A
  • form of intention tremor affecting the upper extremities, head, voice, and other body parts
  • resolves during sleep and often improves w/ alcohol consumption
  • propranolol and primidone are first-line tx
150
Q

chorea

A
  • brief, irregular, unintentional muscle contractions

- movements tend to flow from one to another but are not repetitive or rhythmic

151
Q

athetosis

A

slow, writhing movements that typically affect the hands and feet

  • characteristic of Huntington’s disease
  • chorea and athetosis often occur together
152
Q

akathisia

A

-sensation of restlessness that causes the patient to move frequently

153
Q

Tourette syndrome

A
  • involuntary, stereotyped, repetitive movements and vocalizations called tics
  • common tics: shoulder shrugging, blinking, grimacing, and coprolalia (swearing)
154
Q

Hemiballismus

A

-unilateral, violent arm flinging caused by damage to the contralateral subthalamic nucleus

155
Q

Myoclonus

A
  • involuntary jerking of a muscle or muscle group

- can be rhythmic or patterned and is usually initiated by contraction or relaxation

156
Q

Progressive multifocal leukoencephalopathy

A
  • suspect in an HIV-infected patient w/ focal neuro signs and multiple non-enhancing lesions w/ no mass effect on the CT scan
  • PML is an opportunistic infection caused by the JC virus, a human polyomavirus
  • predominantly involves the cortical white matter, but the brainstem and cerebellum may also be involved
  • hemiparesis and disturbances in speech, vision and gait
157
Q

Cerebral toxoplasmosis

A
  • most common ring-enhancing mass lesion in HIV-infected pts
  • MRI shows multiple, spherical masses in basal ganglia
  • this is unlikely to occur if the patient is receiving trimethoprim-sulfamethoxazole!
  • a positive Toxoplasma serology is quite common in normal subjects in the US, and is NOT specific for this condition
158
Q

Primary CNS lymphoma

A
  • second most common cause of mass lesions in HIV infected pts (behind toxoplasmosis)
  • also presents as a ring-enhancing lesion on MRI, but is usually solitary, weakly enhancing and periventricular
  • the presence of EBV DNA in CSF is quite specific for the diagnosis
159
Q

Subacute sclerosing panencephalitis

A
  • occurs many years after an antecedent measles infection

- CT scan shows scarring and atrophy

160
Q

Idiopathic intracranial hypertension

A
  • typically presents in young, obese women w/ headache, vision changes (blurry vision and diplopia), and pulsatile tinnitus
  • diagnosis involves ocular exam, neuroimaging (MRI, MRV) and LP
  • Papilledema is NOT a contraindication to LP in the absence of obstructive/noncommunicating hydrocephalus or mass lesion
  • CSF analysis is normal in IIH w/ the exception of elevated opening pressure (> 250 mm H2O)
161
Q

Sumatriptan

A

-5-hydroxytryptamine-1 agonist used in the acute tx of migraine headache

162
Q

Timolol eye drops

A
  • used for tx of glaucoma
  • pts present w/ peripheral visual field defects that may appear insidiously or acutely (acute angle-closure glaucoma)
  • pts usually do NOT have positional holocranial headache and abducens nerve palsy (psuedotumor cerebri)
163
Q

alzheimer disease

A
  • early, insidious short-term memory loss
  • language deficits and spatial disorientation
  • later personality changes
164
Q

vascular dementia

A
  • STEPWISE decline
  • early executive dysfunction
  • CEREBRAL INFARCATION and/or deep white matter changes on neuroimaging
165
Q

frontotemporal dementia

A
  • early personality changes
  • apathy, disinhibition and compulsive behavior
  • frontotemporal atrophy on imaging
166
Q

lewy body dementia

A
  • VISUAL HALLUCINATIONS
  • spontaneous PARKINSONISM
  • fluctuating cognition
167
Q

Normal pressure hydrocephalus

A
  • ATAXIA early in disease
  • urinary incontinence
  • dilated ventricles on imaging
168
Q

prion disease

A
  • behavioral changes
  • RAPIDLY PROGRESSIVE (eg over a few months)
  • MYOCLONUS and/or seizures
  • mortality within 1-2 years
169
Q

vascular dementia

A
  • typically presents as a sudden or stepwise decline in executive function w/ mild memory loss early in the disease
  • pts can have focal neurologic deficits on exam, and neuroimaging classically demonstrates cerebral infarction and/or deep white matter changes from chronic ischemia
170
Q

Bell’s palsy

A
  • peripheral neuropathy of CN VII (lesion below the pons)
  • sudden onset of unilateral facial paralysis
  • common findings of the affected side include inability to raise the eyebrow or close the eye, drooping of the mouth corner (with the mouth drawn to the unaffected side), and disappearance of the nasolabial fold
  • pts may also have decreased tearing, hyperacusis, and/or loss of taste sensation over the anterior 2/3 of the tongue
  • lesions in the CNS occurring ABOVE the facial nucleus will typically cause a CONTRALATERAL LOWER facial weakness that SPARES THE FOREHEAD!!!!!!!!!!
  • lesions in the PNS cause weakness of the entire face
  • acute onset of symptoms (
171
Q

Lesions in the CNS occurring above the facial nucleus (above the pons) can result in contralateral hemianesthesia or hemiparesis, and dysarthria. Upper facial weakness can occur w/ central lesions, however these lesions must occur at the level of the facial nucleus or exit the fascicle of the facial nerve at the pontomedullary junction.

A

.

172
Q

Lateral medullary infarct (Wallenberg syndrome)

A
  • occurs due to occlusion of the posterior inferior cerebellar or vertebral artery
  • pts develop loss of pain and temp over the ipsilateral face and contralateral body, ipsilateral bulbar muscle weakness, vestibulocerebellar impairment (eg vertigo, nystagmus), and Horner’s syndrome
  • motor function of the face and body is typically spared
  • acute treatment usually involves IV thrombolytics (eg tPA)
173
Q

lesions of the lateral cerebellar hemisphere

A

-present w/ minimal dizziness and ipsilateral ataxia

174
Q

lateral mid-pontine lesions

A

-affect the motor and principal sensory nuclei of the ipsilateral trigeminal nerve, causing weakness of the muscles of mastication, diminished jaw jerk reflex, and impaired tactile and position sensation over the face

175
Q

medial medullary syndrome (alternating hypoglossal hemiplegia)

A
  • typically due to branch occlusion of the vertebral or anterior spinal artery
  • pts develop contralateral paralysis of the arm and leg and tongue deviation toward the lesion
  • contralateral loss of tactile and position sense can also occur w/ infarcts that extend dorsally
176
Q

medial mid-pontine infarction

A
  • presents w/ contralateral ataxia and hemiparesis of the face, trunk, and limbs (ie ataxic hemiparesis)
  • there is also variable loss of contralateral tactile and position sense
177
Q

Wallenberg syndrome

A

vestibulocerebellar symptoms:
-vertigo, falling to the side of the lesion
-difficulty sitting upright w/o support
-diplopia and nystagmus (horizontal & vertical)
-ipsilateral limb ataxia
sensory symptoms:
-abnormal facial sensation or pain (early sx)
-loss of pain & temp in ipsilateral face and contralateral trunk & limbs
ipsilateral bulbar muscle weakness:
-dysphagia & aspiration
-dysarthria, dysphonia & hoarseness (ipsilateral vocal cord paralysis)
autonomic dysfunction:
-ipsilateral Horner’s syndrome (miosis, ptosis & anhidrosis)
-intractable hiccups
-lack of automatic respiration (esp during sleep)

178
Q

where is the most common site of hypertensive hemorrhages?

A

PUTAMEN (30%)
-the internal capsule that lies adjacent to the putamen is almost always involved, leading to contralateral dense hemiparesis

179
Q

basal ganglia hemorrhage

A
  • contralateral hemiparesis and hemisensory loss
  • homonymous hemianopsia
  • gaze palsy
180
Q

cerebellum hemorrhage

A
  • usually NO hemiparesis
  • facial weakness
  • ataxia and nystagmus
  • occipital headache and neck stiffness
181
Q

Thalamus hemorrhage

A
  • contralateral hemiparesis and hemisensory loss
  • nonreactive miotic pupils
  • upgaze palsy
  • eyes deviate Toward hemiparesis
182
Q

Cerebral lobe hemorrhage

A
  • contralateral hemiparesis (frontal lobe)
  • contralateral hemisensory loss (parietal lobe)
  • homonymous hemianopsia (occipital lobe)
  • eyes deviate away from hemiparesis
  • high incidence of seizures
183
Q

Pons hemorrhage

A
  • deep coma and total paralysis within minutes

- Pinpoint reactive pupils

184
Q

Neurofibromatosis type 1

A
  • cafe-au-lait spots
  • macrocephaly
  • feeding problems
  • short stature
  • learning disabilities
  • pts may later develop fibromas, neurofibromas or different tumors
185
Q

Neurofibromatosis type 2

A
  • bilateral acoustic neuromas

- cataracts

186
Q

Pts w/ acute, severe pain should receive the same standard of pain management regardless of drug hx. IV morphine is appropriate tx for acute, severe pain. Physicians should never undertreat pain, even if there is a risk of abuse. In the case of concern for abuse, frequent reassessment, outpatient follow-up, and referral to a pain specialist is appropriate.

A

.

187
Q

Autism spectrum disorder

A
  • should be suspected in children w/ impaired social communication/interactions and restricted repetitive interests or behaviors
  • comprehensive evaluation includes structured assessments of social, language, and intellectual development in addition to hearing, vision, and genetic testing
188
Q

Alzheimer’s disease

A
  • a MMSE score of less than 24 points is suggestive of dementia
  • initially presents w/ memory symptoms, w/ sx that progress over a period of yrs
  • neuroimaging may demonstrate atrophy which is more prominent in the temporal and parietal lobes, although imaging should primarily be used to exclude alternative causes for dementia as opposed to making a diagnosis of Alzheimer’s
189
Q

social disinhibition and personality changes

A

frontotemporal dementia

190
Q

multi-infarct dementia

A
  • associated w/ focal neurologic signs and evolves in a stepwise fashion
  • multiple hypodense infarcts may be seen on CT
191
Q

Normal pressure hydrocephalus (NPH)

A
  • tried of dementia, gait disturbance and bladder incontinence
  • ventricles are frequently prominent in older pts from volume loss, however the absence of sulcal enlargement can be helpful in differentiating NPH from atrophy
192
Q

Epidural hematomas

A
  • often associated w/ a lucid interval followed by rapid neurological deterioration
  • they appear as a BICONVEX mass on CT scan of the head, and pts w/ features suggestive of deteriorating neurological status or increased ICP require an emergent craniotomy
  • indications for emergent craniotomy: GCS
193
Q

In pts w/ no neurological signs and a small epidrual hematoma, what is the management?

A

a follow-up CT in 24 hours

194
Q

what should you suspect in a patient that presents w/ BILATERAL trigeminal neuralgia?

A

Multiple sclerosis

195
Q

MS

A
  • usually presents during the third or fourth decade w/ recurrent focal neurologic dysfunction
  • that attacks are non-predictable and erratic in presentation
  • sx may last a few weeks w/ variable recovery
  • one of the few conditions that may present w/ bilateral trigeminal neuralgia
196
Q

Huntington chorea

A
  • progressive dementia, which may occur during the third or fourth decade of life
  • autosomal dominant
  • depression, choreiform movements and subcortical dementia
  • CAUDATE atrophy is usually found on CT scan
197
Q

Aseptic meningitis

A
  • usually occurs in the summer months, and is caused by an ECHOVIRUS
  • may present w/ flu-like illness, malaise, vomiting, photophobia, stupor and fever
  • CSF may show elevated WBC
  • diagnosis is made by serology
  • Tx is supportive care
198
Q

TIA

A
  • can present in varied ways affecting the motor, sensory, or ocular system
  • most TIAs are transient and occur due to emboli from the carotid arteries
199
Q

Acute spinal cord compression

A

can present with loss of motor and sensory function, loss of rectal tone, and urinary retention

  • management includes emergent surgical consulation, neuroimaging, and possibly IV glucocorticoids
  • descending corticospinal tracts (lower-extremity weakness and loss of rectal tone)
  • ascending sensory spinothalamic tracts (the sensory level is often 2 spinal cord segments below the level of lesion)
  • descending autonomics in the reticulospinal tract (urinary retention/bladder flaccidity/bladder shock)
200
Q

cauda equina syndrome

A
  • usually unilateral, severe RADICULAR PAIN
  • saddle hypo/anesthesia
  • ASYMMETRIC motor weakness
  • HYPOREFLEXIA/AREFLEXIA
  • late onset bowel and bladder dysfunction
201
Q

Conus medullaris syndrome

A
  • sudden onset severe back pain
  • perianal hypo/anesthesia
  • SYMMETRIC motor weakness
  • HYPERREFLEXIA
  • early onset bowel and bladder dysfunction
202
Q

treatment options for myasthenia gravis

A
  • AChE inhibitors (pyridostigmine, neostigmine; this is the INITIAL TREATMENT CHOICE
  • immunosuppressive agents (prednisone, azathioprine, cyclosporine; steroids are used in pts who show a poor response to AChE inhibitors)
  • thymectomy
203
Q

Edrophonium

A

-short acting AChE inhibitor, used for diagnostic purposes only

204
Q

Atropine

A

-anticholinergic agent that can be used to prevent muscarinic side effects (bradycardia, hypotension, bronchospasm (and hypoxia), increased respiratory secretions,possibly nausea and vomiting) of anticholinesterase therapy in pts w/ myasthenia gravis

205
Q

Plasmapheresis for myasthenia gravis?

A
  • removes ACh receptor antibodies from circulation
  • used in seriously ill pts when other tx are not effective or contraindicated
  • its effect is transient and cannot be used on a long-term basis
  • other indications: stabilization of the patient before thymectomy, myasthenia crisis
206
Q

Muscle weakness

A

-can be due to central or peripheral nervous system disease involving the motor cortex, spinal cord, peripheral nerve, or muscle itself depending on the distribution of findings

207
Q

Myasthenia gravis

A
  • can cause extra-ocular muscle weakness (eg diplopia and ptosis) w/ symmetrical proximal weakness of the extremities (upper more than lower), neck (flexors and/or extensors), and bulbar muscles (eg dysarthria or dysphagia)
  • pts usually have normal reflexes, muscle bulk/tone, and autonomic function. This makes sense because it is NOT a UMN or LMN problem, but rather a NMJ problem in which auto-antibodies attack the ACh Receptor in the post-synaptic membrane
208
Q

Amyotrophic lateral sclerosis

A
  • neurodegenerative disease that is primarily sporadic and more frequently affects men age 40-60
  • pts typically develop upper AND lower motor neuron degeneration leading to asymmetric muscle atrophy, bulbar signs, muscle weakness (distal more than proximal), hyperreflexia, spasticity, and fasciculations
  • sensory abnormalities and ocular deficits are usually absent
209
Q

Electrolyte disturbance (eg sodium, potassium, calcium) can sometimes cause acute neurologic symptoms (eg seizures, weakness, delirium)

A

.

210
Q

Fibromyalgia

A
  • pain disorder characterized by multiple well-defined and localizable tender muscle points
  • pts can present w/ proximal pain-limited weakness but do not usually have ptosis, diplopia, or dysphagia
211
Q

Inflammatory myopathies (eg polymyositis) can present w/ proximal muscle weakness affecting both upper and lower extremities, possible head drop, muscle aches or pains, and dysphagia.

A

.

212
Q

Mononeuropathy

A

-pathology of a single peripheral nerve (eg median neuropathy at wrist, ulnar neuropathy at elbow) that typically presents w/ sensory and/or motor symptoms in the distribution of the affected nerve

213
Q

Polyneuropathy

A
  • peripheral nerve damage (axon and/or myelin) due to conditions such as diabetes mellitus, vitamin B12 deficiency, Guillain-Barre syndrome, or chronic inflammatory demyelinating polyneuropathy (CIDP).
  • pts usually present w/ reduced or absent reflexes, paresthesias, and motor (nonfatigable) and/or sensory symptoms that can involve the upper and/or lower extremities
  • however, bulbar muscles are less commonly affected (except in GBS and CIDP)
214
Q

Statin-induced myopathy

A
  • can present w/ proximal muscle weakness and myalgias
  • pts typically do NOT have fatigable weakness, involvement of the eyelids, ocular dysmotility, or swallowing difficulties
215
Q

Thyroid-related myopathy

A
  • can present w/ proximal muscle weakness and diplopia (restrictive ophthalmopathy)
  • thyroid-related eye disease (eg Graves’ disease) can lead to proptosis, lid retraction, and diplopia (usually not fatigable)
  • they typically do NOT cause dysphagia or bilateral ptosis
216
Q

Creutzfeldt-Jakob disease

A
  • rapidly progressive dementia, myoclonus and sharp, triphasic, synchronous discharges on EEG
  • this spongiform encephalopathy is caused by a prion
  • most pts die within one year of symptom onset
217
Q

Huntington’s dementia

A
  • defect in an autosomal dominant gene ON CHROMOSOME 4
  • striatal neuro-degeneration
  • early onset dementia (35-50 yrs old), progressive choreiform movement of all limbs, grimacing, and ataxic gait
218
Q

Parkinson’s disease

A
  • progressive loss of nigrostriatal dopaminergic neurons

- bradykinesia, resting pill rolling tremor, cogwheel rigidity, shuffling gait and masked facies

219
Q

Alzheimer’s dementia

A
  • amyloid plaques
  • neurofibrillary tangles
  • selective loss of CHOLINERGIC neurons
220
Q

Pick’s disease

A
  • neurodegenerative disease of frontal and temporal lobes
  • resembles Alzheimer’s dementia clinically, but is more commonly seen in FEMALES
  • onset of symptoms is around 50 years of age
  • personality and language changes are often more prominent than cognitive symptoms
221
Q

Acute angle-closure glaucoma

A
  • commonly occurs as a response to pupillary dilation from medications (eg anticholinergics, sympathomimetics) or another stimulus (eg dim light).
  • pts typically develop unilateral orbitofrontal headache associated w/ nausea/vomiting, unilateral eye pain w/ conjunctival injection, and a dilated pupil w/ poor light response
  • untreated pts can develop permanent vision loss within 2-5 hours of symptoms onset!!
  • more common in women (esp age > 40), asian and inuit population, and those w/ farsightedness
222
Q

Cluster headaches

A
  • more common in men

- last

223
Q

Herpes zoster ophthalmicus

A

-generally presents less acutely and may be accompanied by a unilateral rash in the trigeminal distribution

224
Q

how do intracranial tumors commonly present?

A

-insidious onset of headache over weeks to months, occasionally w/ focal neurologic changes

225
Q

what is the ESR usually in pts w/ temporal arteritis?

A

ESR > 50 mm/h

226
Q

optic neuritis

A
  • acute vision loss, pain, afferent pupillary defect

- most commonly occurs in women

227
Q

Exertional heat stroke

A

risk factors: strenuous activity during hot and humid weather, dehydration, poor acclimatization, lack of physical fitness, obesity, anticholinergics, antihistamines, phenothiazines, tricyclics
clinical manifestations: core temp > 40C (104F) immediately after COLLAPSE AND:
-CNS dysfunction (AMS, confusion, irritability, seizure)
-Additional organ or tissue damage (renal/hepatic failure, DIC, ARDS)
Management: rapid cooling preferably with ICE WATER IMMERSION (can consider high flow cool water dousing, ice/wet towel rotation, evaporative cooling), fluid resuscitation, electrolyte correction, management of end-organ complications, NO ROLE FOR ANTIPYRETIC THERAPY

228
Q

difference between heat exhaustion and heat stroke?

A

-both have a body temp > 104F, but heat stroke also has CNS dysfunction (confusion, irritability, seizure, etc.)

229
Q

when is evaporative cooling preferred over ice water immersion for heat stroke?

A

-evaporative cooling is preferred in NONEXERTIONAL or CLASSIC heat stroke (seen in elderly pts w/ underlying comorbidities that limit their ability to cope w/ excessive heat) as ice water immersion is associated w/ higher morbidity and mortality in these pts

230
Q

Brain abscess

A
  • headache, focal neurologic deficity, and ring-enhancing intracranial lesion(s) on contrast CT of brain in an immunocompetent patient w/ an adjacent bacterial infection
  • fever is present in only 50% of cases
  • Viridans streptococci and other head-and-neck anaerobes are the most common pathogens when brain abscess results from sinusitis
  • 25% of cases result from hematogenous spread from distant infections, usually lung infections or endocarditis; in these cases gram-negatives and Staph aureus are most common
  • in rare cases of direct inoculation from trauma or surgery, Staphylococcus predominates
  • Tx: PROLONGED (4-8 week minimum) antibiotic therapy and ASPIRATION/DRAINAGE
231
Q

can brain neoplasms present as ring-enhancing lesions on contrast CT?

A

YES!!

232
Q

Rhizopus species

A
  • cause of MUCORMYCOSIS and can cause cerebral infection due to direct extension of rhino-sinusitis
  • causes infection in IMMUNOCOMPROMISED pts and those w/ poorly controlled diabetes
233
Q

Cerebral toxoplasmosis

A

ring-enhancing lesions in pts w/ AIDS

-usually multiple lesions and tend to occur in the basal ganglia and at the cortical grey-white matter interface

234
Q

what is the most effective symptomatic therapy for parkinsonism? What are the side effects?

A

Levodopa/carbidopa

  • the most common early side effects are hallucinations, dizziness, headache, and agitation
  • after several years of therapy, involuntary movements are more likely to occur
235
Q

side effect of COMT inhibitors for parkinsonism (entacapone, tolcapone)

A

Choreiform dyskinesia

236
Q

side effect of amantadine for parkinsonism

A

Livedo reticularis

237
Q

side effect of anticholinergics (eg benztropine) used in parkinsonism

A

urinary retention

-they improve tremor and rigidity but do NOT have much effect on bradykinesia

238
Q

Spinal cord compression

A
  • characterized by signs and symptoms of UMN dysfunction distal to the site of compression
  • these include weakness, hyperreflexia, and an extensor plantar response
  • cord compression is a medical emergency requiring prompt diagnosis by spinal MRI
239
Q

Lyme disease

A
  • typically presents as erythema migrans, headache, arthralgias, and myalgias
  • late disseminated disease that occurs months to years after infection can manifest as subacute encephalopathy (meningitis/encephalitis) and axonal polyneuropathy
240
Q

Guillain-Barre syndrome is NOT characterized by UMN signs or significant sensory findings (except in rare sensory forms)

A

.

241
Q

Guillain-Barre syndrome (GBS)

A
  • ascending weakness, bulbar symptoms (eg dysarthria, dysphagia) and respiratory compromise after antecedent illness such as respiratory or GI infection (esp Campylobacter jejuni)
  • CSF analysis shows ALBUMINOCYTOLOGIC DISSOCIATION
  • Tx: IVIG or Plasmapheresis
  • Monitor autonomic (eg arrhythmias, orthostatic hypotension, urinary retention, ileus, lack of sweating) and respiratory functions
242
Q

MG

A
  • ocular symptoms (eg ptosis, diplopia) and fluctuating muscle weakness that is worse late in the day
  • deep tendon reflexes are normal
  • cyclosporine and pyridostigmine for treatment
243
Q

Tx of herpes simplex encephalitis

A

IV acyclovir

244
Q

role of glucocorticoids in tx of guillain-barre syndrome?

A

studies have shown they are NOT beneficial, and so they are no longer recommended

245
Q

tx of ALS

A

Riluzole

246
Q

acute and long term treatment of MS?

A
  • acute exacerbation: high dose IV corticosteroids
  • long term: beta-interferon, glatiramer acetate, plasmapheresis, cyclophosphamide, IVIG
  • beta-interferon or glatiramer acetate is used to decrease the frequency of exacerbations in pts w/ relapsing-remitting or secondary progressive form of MS
247
Q

spinal epidural abscess

A
  • risk factors: IV drug use, immunocompromised state (eg diabetes, HIV, alcoholism), infectious spread from contiguous/distant source, spinal trauma or surgery
  • clinical features: classic triad (fever, severe FOCAL back pain and neurologic deficits), progressive symptoms (radiculopathy, motor & sensory deficits, bowel or bladder dysfunction & eventual paralysis)
  • management: CBC, ESR/CRP, Blood cultures, MRI OF SPINE W/ GADOLINIUM CONTRAST, CT-guided aspiration/biopsy, Empiric antibiotics, surgical decompression
  • Antibiotics along w/ emergency surgical decompression and drainage of the abscess are recommended for most patients
  • Staph aureus accounts for about 60% of infections caused by pyogenic bacteria
248
Q

Herpes simplex virus (HSV) encephalitis

A
  • mainly affects the temporal lobe of the brain

- may present acutely (

249
Q

Cryptococcal meningitis

A
  • often seen in immunocompromised patients (eg HIV) and is uncommon in immunocompetent patients
  • CSF: elevated opening pressure, low leukocytes (mononuclear predominance), slightly elevated proteins, and low glucose
  • organisms can be detected by INDIA INK PREPARATION
250
Q

Craniopharyngioma

A
  • benign suprasellar tumors that arise from Rathke’s pouch
  • usually present w/ signs of hypopituitarism, headaches, and bitemporal blindness
  • bimodal age distribution: children and 55-65 age group
  • in children, retarded growth is most prominent feature; in adults, sexual dysfunction is most prominent; women may have amenorrhea
  • Tx: surgery and/or radiotherapy
251
Q

Optic neuritis

A
  • may be monocular or binocular depending on the cause

- usually associated w/ loss of central vision (scotomas) and an afferent pupillary defect

252
Q

The behavioral variant of frontotemporal dementia

A
  • differentiated from other dementing illnesses by early personality changes and compulsive behaviors, earlier age of onset, and a strong hereditary component
  • aka Pick’s disease
253
Q

Alzheimer disease

A
  • progressive dementia that typically begins w/ memory loss, language difficulties, and apraxia, followed by impaired judgement and personality changes in the late stages
  • risk factros: advanced age, female gender, family hx, head trauma, and Down syndrome
  • Tx: psychosocial intervention and pharmacotherapy w/ AChE inhibitors (eg donepezil, galantamine, rivastigmine) and/or the NMDA antagonist MEMANTINE
254
Q

Dementia w/ Lewy Bodies

A
  • early presentation of VISUAL HALLUCINATIONS accompanied by fluctuating cognition w/ variations in attention and alertness (often leading to misdiagnosis as delirium)
  • complex, highly detailed visual hallucinations may occur
  • Parkinsonism may also occur, but it responds poorly to dopaminergic agonist therapy
255
Q

Neurosyphilis

A

-appears in 15-20% of late syphilis cases and can present w/ forgetfulness, personality change, dysarthria, and intention tremor

256
Q

Vascular dementia

A

-accounts for 15-20% of dementia cases

-

257
Q

blood supply to brain

A
  1. anterior vasculature is comprised of the internal carotid artery and its branches, especially the paired anterior and middle cerebral arteries
  2. posterior circulation is comprised of the paired vertebral arteries, which unite to form the basilar artery that then further divides into the paired posterior cerebral arteries
258
Q

anterior cerebral stroke

A
  • contralateral motor or sensory deficits, which are more pronounced in the lower limb than the upper limb
  • urinary incontinence can also be seen, gait dyspraxia, primitive reflexes (grasp, suck), abulia, and emotional disturbances.
259
Q

lacunar infarcts

A
  • small vessel infarcts typically affecting the deep subcortical structures
  • caused by occlusion of a single, deep-penetrating branch of a large cerebral artery
  • well-recognized syndromes: pure motor hemiparesis, pure sensory stroke, sensorimotor, dysarthria-clumsy hand, and ataxic hemiparesis
  • the face, arm, and leg are all equally affected w/ sensorimotor lacunar stroke, and there are no associated cortical symptoms (ie, no urinary incontinence)
260
Q

middle cerebral artery (MCA) stroke

A
  • contralateral motor and/or somatosensory deficits (more pronounced in the face or upper limb than lower limb), and homonymous hemianopia or quadrantanopia
  • if the dominant lobe (left) is involved, a patient may have APHASIA; if the nondominant lobe (right) is involved, a patient may have HEMINEGLECT or ANOSOGNOSIA (lack of awareness regarding one’s illness)
261
Q

Occlusion of the internal carotid artery

A
  • supplies the anterior circulation, generally results in extensive neurologic deficits as both the MCA and ACA territories are affected
  • sx include dense, contralateral hemiplegia (face, arm, and leg equally affected) w/ contralateral sensory, visual, language, or spatial impairments
262
Q

Posterior cerebral artery stroke

A

-homonymous hemianopia, alexia w/o agraphia (dominant hemisphere), visual hallucinations (calcarine cortex), sensory sx (thalamus), third nerve palsy w/ paresis of vertical and horizontal eye movements, and contralateral motor deficits (cerebral peduncle, midrain)

263
Q

posterior limb of internal capsule (lacunar infarct) lesion

A
  • unilateral MOTOR impairment
  • NO sensory or cortical deficits
  • NO visual field abnormalities
264
Q

MCA occlusion

A
  • CONTRALATERAL somatosensory AND MOTOR DEFICIT (face, arm, and leg
  • conjugate eye deviation TOWARD SIDE OF INFARCT
  • homonymous hemianopia
  • aphasia (dominant hemisphere)
  • hemineglect (nondominant hemisphere)
265
Q

ACA occlusion

A
  • contralateral somatosensory and motor deficit, predominantly in lower extremity
  • abulia (lack of will or initiative)
  • dyspraxia, emotional disturbances, urinary incontinence
266
Q

vertebrobasilar system lesion (supplying the brain stem)

A
  • alternate syndromes w/ contralateral hemiplegia and IPSILATERAL cranial nerve involvement
  • possible ataxia
267
Q

Thiamine deficiency

A
  • can cause Wernicke’s encephalopathy (encephalopathy, oculomotor dysfunction (nystagmus, conjugate gaze palsy), and gait ataxia)
  • this condition may be induced iatrogenically in susceptible pts by administration of glucose without thiamine!
  • chronic thiamine (B1) deficiency can also cause Korsakoff’s syndrome, characterized by irreversible amnesia, confabulation, and apathy
  • pathogenesis involves dietary deficiency, impaired utilization, and poor GI absorption
268
Q

Cerebellar infarction

A
  • medial vermis causes severe vertigo and nystagmus

- lateral hemispheres cause dizziness, ataxia, and weakness

269
Q

basal ganglia hemorrhage

A
  • contralateral hemiparesis and hemisensory loss
  • homonymous hemianopsia
  • gaze palsy
270
Q

cerebellum hemorrhage

A
  • usually NO hemiparesis
  • facial weakness
  • ataxia and nystagmus
  • occipital headache and neck stiffness
271
Q

Thalamus hemorrhage

A
  • contralateral hemiparesis and hemisensory loss
  • nonreactive miotic pupils
  • upgaze palsy
  • eyes deviated Towards hemiparesis
272
Q

cerebral lobe hemorrhage

A
  • contralateral hemiparesis (frontal lobe)
  • contralateral hemisensory loss (parietal lobe)
  • homonymous hemianopsia (occipital lobe)
  • eyes deviate AWAY from hemiparesis
  • high incidence of seizures
273
Q

Pons hemorrhage

A
  • deep coma and total paralysis within minutes

- Pinpoint reactive pupils

274
Q

Deep intracranial hemorrhage (eg basal ganglia, cerebellum, thalamus, pons) is typicall due to HYPERTENSIVE VASCULOPATHY. Lobar hemorrhage is more often associated w/ AMYLOID ANGIOPATHY (esp in elderly). Eyes may deviated toward the side of hemiparesis in pts w/ thalamic hemorrhage, helping to differentiate it from other sites of intracranial hemorrhage.

A

.

275
Q

Normal pressure hydrocephalus (NPH)

A
  • thought to result from DECREASED CSF ABSORPTION or transient increases in intracranial pressure that cause permanent ventricular enlargement w/o chronically increasing ICP.
  • characterized by dementia, gait disturbances, and incontinence
276
Q

Pts w/ acute arterial occlusion (limb ischemia)

A
  • classically present w/ the “5 P’s”: Pain, Pallor, Pulselessness, Paresthesia, and Paralysis
  • immediate anticoagulation w/ heparin and referral for emergency vascular surgery evaluation should be performed in those w/ suspected limb ischemia
277
Q

what should you consider in all pts who present w/ acute delirium or acute ataxia, esp. malnourished and alcoholic pts?

A
  • Wernicke’s encephalopathy (confusion, ataxia, ophthalmoplegia)
  • give thiamine!
  • if history is limited, the goal should be to treat potentially reversible causes of confusion: thiamine, dextrose, supplemental oxygen, naloxone
278
Q

opiate antagonist used to treat opiate overdose?

A

naloxone

279
Q

competitive antagonist of the GABA receptor, used to reverse benzodiazepine overdose?

A

Flumazenil

280
Q

first-line tx for hypertensive encephalopathy?

A

nitroprusside

labetalol

281
Q

Fatigable muscle weakness that primarily involves the extraocular and bulbar musculature is most consistent with what?

A

Myasthenia gravis

-approx. 15% of MG also have a coexisting THYMOMA, thus, screening CT of the chest is recommended

282
Q

Cerebellar degeneration

A
  • common among chronic alcohol abusers

- symptoms: gait instability, truncal ataxia, difficulty w/ rapid alternating movements, hypotonia, and intention tremor

283
Q

Neoplasms of the cerebellopontine angle (eg, acoustic schwannoma) can cause cerebellar dysfunction, vestibular dysfunction, and hearing loss.

A

.

284
Q

signs and symptoms of anticholinergic toxicity

A
  • “red as a beet, dry as a bone, hot as a hare, blind as a bat, mad as a hatter, and full as a flask”
  • flushing, anhidrosis/dry mouth, hyperthermia, mydriasis/vision changes, delirium/confusion, urinary retention/constipation, headache, dizziness, tachycardia
  • can precipitate acute glaucoma
285
Q

Levodopa

A
  • med used for Parkinson’s disease
  • nausea and vomiting are seen in 80% of pts if carbidopa is not also given
  • ANXIETY AND AGITATION are central effects of dopamine that occur regardless of whether carbidopa is added or not
286
Q

Selegiline

A
  • MAO-B inhibitor used in tx of Parkinson’s
  • co-administration w/ SSRIs and/or TCA’s can precipitate serotonin syndrome, which is characterized by agitation, confusion, tachycardia, muscle rigidity, and sometimes seizures
287
Q

Bromocriptine

A
  • dopamine agonist used in tx of Parkinson’s

- side effects: hypotension, nausea, constipation, headaches, dizziness

288
Q

Propranolol

A
  • NON-selective beta blocker used most often to treat benign essential tremor and portal hypertension
  • NOT indicated for use in Parkinson’s didase
  • side effects: bradycardia, hypotension, somnolence, and impotence
289
Q

levothyroxine

A
  • used to treat hypothyroidism

- side effects: tremor, anxiety, tachycardia, weight loss, and diarrhea

290
Q

Trihexyphenidyl and Benztropine are both ANTICHOLINERGICS used in treatment of Parkinson’s

A

.

291
Q

Ischemic (thrombotic) stroke

A
  • atherosclerotic risk factors (uncontrolled HTN, diabetes), +/- hx of TIA
  • local in-situ obstruction of an artery
  • sx often fluctuate- stuttering progression w/ periods of improvement
292
Q

Ischemic (embolic) stroke

A
  • hx of cardiac disease (a. fib, endocarditis) or carotid atherosclerosis (bruit)
  • onset of symptoms is ABRUPT and USUALLY MAXIMAL AT THE START
  • multiple infarcts within different vascular territories
293
Q

Intracerebral hemorrhage stroke

A
  • hx of uncontrolled HTN, coagulopathy, illicit drug use (amphetamines, cocaine)
  • sx progress over minutes to hours
  • focal neuro sypmtoms appear early, followed by features of increased ICP (vomiting and headache, bradycardia, reduced alertness)
294
Q

spontaneous subarachnoid hemorrhage

A
  • rupture of an arterial saccular (“berry”) aneurysm or from an AV malformation
  • severe headache at onset of neurologic symptoms
  • meningeal irritation
  • focal deficits UNCOMMON
295
Q

Hypertensive intracranial hemorrhages

A
  • most commonly in the basal ganglia (PUTAMEN!!), thalamus, pons, and cerebellum
  • pts tend to present intitially w/ focal symptoms but can rapidly progress to signs of elevated ICP
296
Q

Multiple sclerosis (MS)

A
  • usually presents w/ >2 distinctive episodes of CNS dysfunction w/ at least some resolution
  • T2 weighted MRI shows multifocal ovoid subcortical white matter lesions located in periventricular, juxtacortical, infratentorial, or spinal cord areas
  • CSF shows normal pressure and the presence of oligoclonal IgG bands in >95% of pts
297
Q

antibodies in MS

A

myelin oligodendrocyte glycoprotein and myelin basic protein

-however, these are NOT specific for MS

298
Q

Riluzole

A
  • glutamate inhibitor that is currently approved for use in pts w/ amyotrophic lateral sclerosis (ALS)
  • note, it may prolong survival and the time to tracheostomy
  • side effects: dizziness, nausea, weight loss, elevated liver enzymes, skeletal weakness
299
Q

tx for acute exacerbations of MS? of Guillain-Barre?

A

MS: corticosteroids
GBS: IVIG and plasmapharesis

300
Q

Chemotherapy-induced peripheral neuropathy

A
  • symmetric, distal, SENSORY neuropathy that spreads in a stocking-glove pattern
  • common causative agents: platinum-based meds (cisplatin), taxanes (paclitaxel), and Vinca alkaloids (vincristine)
301
Q

Tabes dorsalis

A
  • manifestation of late neurosyphilis that involves the posterior spinal columns and dorsal roots
  • usually presents w/ sensory ataxia, brief stabbing pains, and is associated w/ pupillary irregularities (eg Argyll-Robertson pupil)
302
Q

Parkinson’s disease should be suspected in pts w/ a resting tremor of 4-6 Hz that is asymmetric and associated w/ rigidity. Tremor is often the presenting symptom of Parkinson disease. Trihexyphenidyl is an anticholinergic (along w/ benztropine) med sometimes used in the tx of Parkinson’s disease, generally in YOUNGER PTS WHERE TREMOR IS THE PRIMARY SYMPTOM.

A

.

303
Q

Early use of aspirin (eg within 48 hours) in acute ischemic stroke due to atherosclerotic thrombosis or embolism is associated w/ a lower risk of recurrent stroke and decreased mortality. Conversely, early use of IV heparin is generally NOT recommended as it is associated w/ an increased risk of symptomatic intracranial hemorrhage.

A

.

304
Q

IV antibiotics decrease the risk of septic embolic events in pts w/ native valve infective endocarditis! Surgery can be considered in pts w/ significant valvular dysfunction, persistent/difficult to treat infection, or recurrent embolism

A

.

305
Q

Hypothyroidism

A
  • an important cause of reversible changes in memory and mentation.
  • it will be accompanied by systemic changes such as weight gain, fatigue, and constipation
306
Q

Alzheimer’s dementia

A
  • early problems in visuospatial abilities (eg getting lost in their neighborhood) and anterograde memory formation
  • old memories tend to be preserved
  • personality and behavioral changes (hypersexuality, agitation) may occur as the disease progresses
  • hallucinations and changes in alertness are late findings
307
Q

Lewy body dementia

A
  • presents w/ alterations in alertness, visual hallucinations, and extrapyramidal symptoms
  • memory deficits occur later in the course of disease
308
Q

Vascular dementia

A
  • step wise deterioration as damage from multiple strokes slowly adds up
  • risk factors for vascular disease, hx of cerebrovascular disease, and imaging evidence of strokes
  • psychiatric disturbances such as depression and agitation are common
309
Q

Huntington’s disease

A
  • autosomal dominant
  • neurodegenerative disease affecting the caudate and putamen
  • mean age of onset is 35-44 years of age
  • sx: choreathetoid movements, behavioral disturbances, and dementia
310
Q

Chronic subdural hematomas

A
  • more common in elderly and alcoholics due to decreased brain volume and propensity for falls
  • present insidiously w/ decreased consciousness, headache, cognitive and memory deficits, balance problems, aphasia, or motor deficits
311
Q

pseudodementia

A
  • presentation of major depression in the elderly

- depressed pts may have memory changes and other symptoms concerning for dementia

312
Q

NPH

A
  • dementia, abnormal gait, and urinary incontinence

- gait is broad-based and shuffling and pts tend to be bradykinetic

313
Q

Vitamin B12 deficiency

A
  • dementia w/ megaloblastic anemia and posterior spinal column deficits
  • the most common cause is pernicious anemia
314
Q

Thiamine deficiency

A
  • can lead to Wernicke-Korsakoff syndrome
  • presents as ataxia, ophthalmoplegia, and confusion (Wernicke’s) in addition to confabulation and amnesia (Korsakoff’s)
  • particularly common in alcoholics
315
Q

Unilateral foot drop

A
  • characterized by a “steppage” gait: exaggerated hip and knee flexion while walking
  • common causes include L5 radiculopathy and compression peroneal neuropathy
  • L5 radiculopathy may also have weak foot inversion and plantar flexion, while these will be normal in peroneal neuropathy
316
Q

lesion in the basal ganglia cause what kind of gait?

A

-slow shuffling gait (Parkinson’s)

317
Q

cerebellar ataxia

A
  • can result from lesions of the vermis (truncal ataxia) or the cerebellar hemispheres (limb ataxia)
  • features include staggering and swaying from side to side, impaired tandem gait and titubation (truncal tremor)
318
Q

gait in pyramidal tract or corticospinal tract lesions

A
  • spastic ataxia
  • gait appears stiff or rigid w/ circumduction (the spastic leg is abducted and advanced while in extension and internal rotation) and plantar flexion of the affected limb
319
Q

damage to the cortico-cortical white matter fibers of the frontal lobe, as seen in NPH, can lead to what type of gait?

A
  • gait apraxia (Bruns ataxia)
  • strength, coordination, and sensory function are intact, but there is difficulty in initiation of forward movement of the feet when they are in contact w/ the ground (“magnetic gait”)
320
Q

Pts w/ loss of proprioception due to sensory neuronopathy may have postural or gait instability and a WIDE-BASED GAIT. Pts may stomp their feet against the floor (slap gait) to help them know where their lower limbs are relative to the ground.

A

.

321
Q

gait in vestibular disorder

A
  • unsteady, falling to one side
  • normal sensation, reflexes and motor strength; nausea and vertigo are usually present
  • causes: acute labyrinthitis, Meniere disease
322
Q

Donepezil is an acetyl-cholinesterase inhibitor used in the tx of Alzheimer dementia. A key distinguishing factor is that pts w/ pseudodementia are frequently distressed by their impaired memory; those w/ Alzheimer dementia are often relatively unconcerned and confabulate. When depression w/ pseudodementia is suspected, tx w/ antidepressants is the first step, w/ expected improvement in cognitive symptoms. If depression improves but cognitive deficits persist, a diagnosis of Alzheimer disease and treatment w/ donepezil should be considered.

A

.

323
Q

Depression w/ pseudodementia should be considered in the differential diagnosis of elderly pts w/ cognitive impairment and depressive symptoms. Antidepressants are the tx of choice and should result in reversal of cognitive deficits.

A

.

324
Q

CSF of MS pts?

A
  • IgG oligoclonal bands are present in 85-90% of cases of multiple sclerosis
  • CSF pressure, protein and cell count are grossly normal
  • note that elevated Ig levels may be found in other diseases, and so the presence of oligoclonal bands is NOT considered diagnostic for MS
325
Q

CSF finding in Guillain Barre syndrome?

A

albumino-cytologic (elevated protein and normal cell count) dissociation

326
Q

Dementia w/ Lewy bodies

A
  • alterations in alertness (fluctuating), visual hallucinations, and extrapyramidal symptoms
  • “Lewy bodies” are eosinophilic intracytoplasmic inclusions representing accumulations of ALPHA-SYNUCLEIN PROTEIN, and may be seen in the neurons of the substantia nigra, locus ceruleus, dorsal raphe, and substantia innominata
  • tx: AChE inhibitor like rivastigmine; for hallucination refractory to AChE inhibitors, atypical antipsychotics may be of benefit
327
Q

Key distinction between Lewy body dementia and Parkinson’s disease?

A

Lewy bodies are found in both.
-the key distinction is the early appearance of dementia in Lewy body disease and of motor symptoms in Parkinson’s disease

328
Q

pathologic hallmarks of Alzheimer’s dementia?

A

-Neurofibrillary tangles and senile plaques

329
Q

pathophysiology of NPH?

A

-impaired CSF absorption

330
Q

Demyelinating diseases typically present w/ both sensory AND motor deficits!!

A

.

331
Q

Generalized seizures

A
  • appears to involve both hemispheres of brain
  • can have loss of consciousness
  • bilateral motor findings
  • can be convulsive or nonconvulsive (absence)
332
Q

partial seizures

A
  • limited to part of 1 hemisphere of brain
  • simple partial seizures: no loss of consciousness, feeling of familiarity (deja-vu), can have aura, patient may remember event well
  • partial seizures w/ generalization: loss of consciousness, tonic-clonic activity
  • complex partial seizures: loss of consciousness, can have aura, more automatisms (eg chewing, swallowing, sucking), sometimes have bilateral motor findings
333
Q

Partial seizures arise from a discrete focus in the brain, and generalized seizures involve the brain diffusely from the beginning of the event.

A

.

334
Q

seizures with aura’s are indicative of a PARTIAL seizure arising from a specific focus in the brain.

A

.

335
Q

Childhood absence seizures (generalized nonconvulsive seizures)

A
  • generally present as multiple short episodes of staring and behavioral arrest that can sometimes mimic a complex partial seizure
  • generally associated w/ minimal to NO postictal state and are much shorter in duration that complex partial seizures
  • they rarely evolve into generalized tonic-clonic seizures
336
Q

Diffuse muscle soreness, significantly elevated creatine kinase levels, urinary incontinence, and initial “aura” make partial seizure w/ secondary generalized tonic-clonic convulsion more likely than simple or complex partial seizure

A

.

337
Q

Lennox-Gastaut syndrome

A

-can present w/ a variety of different seizure types, but pts are usually age

338
Q

Loss of consciousness is seen w/ complex partial seizures and partial seizures w/ secondary generalization but NOT simple partial seizures. Pts w/ COMPLEX PARTIAL SEIZURES typically have AUTOMATISMS during their LOSS OF CONSCIOUSNESS; these activities include chewing, picking movements of the hands, and lip smacking.

A

.

339
Q

a lesion in the posterior limb of the internal capsule is characterized by what?

A
  • unilateral motor weakness of the face, arm, and leg WITHOUT any higher cortical dysfunction or visual field abnormalities
  • lesions in the vertebrobasilar system that supply the BRAINSTEM are characterized by “ALTERNATE” SYNDROMES, with contralateral hemiplegia and ipsilateral cranial nerve involvement!
340
Q

Most common lacunar syndromes (from stroke)?

A
  • pure motor hemiparesis, pure sensory syndrome, ataxic hemiparesis, sensorimotor syndrome, and dysarthria-clumsy hand syndrome
  • pute motor strokes can occur in the subcortical white matter or brainstem
  • pure sensory strokes typically occur in the thalamus
  • ataxia-hemiparesis generally occurs with strokes in the pons
341
Q

Anterior cerebral artery occlusion

A
  • supplies the medial aspect of the cerebral hemisphere
  • causes contralateral somatosensory and motor weakness that predominantly affects the lower extremity
  • associated findings: dyspraxia, abulia, emotional disturbances, and urinary incontinence
342
Q

Lesions in the vertebrobasilar system that supply the brainstem

A
  • characterized by “alternate” syndromes, w/ contralateral hemiplegia and ipsilateral cranial nerve involvement
  • in mid-brain stroke, there will be ipsilateral oculomotor paralysis w/ contralateral ataxia or hemiplegia
343
Q

MCA occlusion

A

-contralateral somatosensory and motor weakness (face, arm, and leg), conjugate eye deviation toward the side of the infarct, Broca’s expressive aphasia (if dominant side is affected), homonymous hemianopia, and hemineglect (nondominant side lesion)

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