Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Internal Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

Diabetic CN III Neuropathy

A
  • Ischemic deficit (not compression) affecting somatic fibers only.
  • CN III has both somatic and parasympathetic fibers which have different blood supplies.

Somatic fibers: innervates superior, inferior, and medial rectus, inferior oblique, and levator palpebrae

Parasympathetic fibers: innervates the sphincter of the iris and ciliary muscle —–> fixed, dilated pupil and loss of accomodation

Symptoms: “down and out” gaze, ptosis (unopposed action of the lateral rectus and superior oblique)
- Intact pupillary response and accommodation.

  • Compression neuropathy affects all functions.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Todd’s palsy

A

preceded by a focal motor seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Carotid artery thrombosis

A
  • Most commonly affects the middle cerebral a. —> contralateral hemiparesis and hemianesthesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Lacunar stroke - pure motor hemiparesis

A
  • Lacunar infarction in the posterior limb of the internal capsule

Presentation: unilateral motor deficit (face, arm, and to a lesser extent leg), mild dysarthria
- No loss of sensory, visual, or higher cortical function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Lacunar stroke - pure sensory stroke

A
  • Stroke in the ventroposterolateral nucleus of the thalamus.

Presentation: unilateral numbness, parasthesias and hemisensory deficit involving the face, arm, trunk, and leg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Lacunar stroke - ataxic hemiparesis

A

Lacunar infarction of the anterior limb of the internal capsule

Presentation: weakness that is more prominent in the lower extremity, along with ipsilateral arm and leg incoordination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lacunar stroke - dysarthria-clumsy hand syndrome

A

Lacunar stroke at the basis of the pons

Presentation: hand weakness, mild motor aphasia
- NO sensory abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Migraine treatment and prophylaxis

A

Antiemetics: prochlorperazine, chlorpromazine, and metaclopramide

  • NSAIDS or triptans if started early into the headache.

Prophylaxis: amitriptyline, propranolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Basal ganglia hemorrhage

A

Symptoms: contralateral hemiparesis and hemisensory loss, homonomyous hemianopsia, gaze palsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cerebellar hemorrhage

A
  • Usually NO hemiparesis

- Facial weakness, ataxia, nystagmus, occipital headache, and neck stiffness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Thalamic hemorrhage

A

Symptoms: contralateral hemiparesis and hemisensory loss, non-reactive miotic pupils, upgaze palsy, eyes deviate towards hemiparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cerebral lobe hemorrhage

A

Symptoms: Contralateral hemiparesis (frontal lobe), contralateral hemisensory loss (parietal lobe), homonymous hemianopsia (occipital lobe), eyes deviate away from hemiparesis, high incidence of seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pons hemorrhage

A

Symptoms: deep coma and total paralysis within minutes, pinpoint reactive pupils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Essential tremor

A
  • Bilateral action tremor of the hands, usually without leg involvment
  • Possible isolated head tremor without dystonia(involuntary repetitive movement)
  • Relieved with alcohol
  • no other neurologic defecits.

Treatment: propranolol; second-line: primidone and topiramate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Parkinson’s disease tremor

A
  • resting tremor (4-6Hz) that decreases with voluntary movement
  • Usually involves legs and hands
  • facial involvement less common
  • May progress to involve other areas of the body

Tetrad: resting tremor, rigidity, postural instability, and bradykinesia

  • Tremor worsens when performing mental tasks and disappears with movement
  • Due to progressive loss of dopaminergic neurons in the basal ganglia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cerebellar tremor

A
  • Usually associated with ataxia, dysmetria (lack of accuracy during voluntary movement), or gait disorder
  • Tremor increases steadily as hand reaches its target

-Can see postural, action, or intention tremors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Physiologic

A
  • Low amplitude (10-12Hz), not visible under normal conditions
  • acute onset with sympathetic activity (drugs, hyperthyroidism, caffeine)
  • Usually worse with movement and can involve the face and extremities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Brain death

A
  • Absent cortical and brainstem function
  • Spinal cord may still be functioning, so DTR can still be present.
  • HR becomes invariant due to loss of vagal control.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Status epilepticus

A
  • single seizure lasting longer than 30 mins
  • Brains that have seized for >5 minutes are at risk of permanent injury due to excitatory cytotoxicity —-> cortical laminar necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Neurofibromatosis type 2

A
  • mutation in tumor suppressor gene on chromosome 22
  • Subcutaneous neurofibromas, cafe-au-lait spots, deafness due to acoustic neuromas

severe variant - Wishart - framshift or nonsense mutations
milder variant - Gardner - missense or splice-site mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Primary sclerosing cholangitis

A

Clinical features: fatigue, pruritis
- 90% of pts have underlying IBS, mainly ulcerative colitis

Labs: Aminotransferases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Ascited Fluid Characteristics

A

Neutrophils: 250 peritonitis (secondary or spontaneous)

Total protein: >or= 2.5 (high-protein ascites) - CHF, constrictive pericarditis, peritoneal carcinomatosis, TB, Budd-Chiari syndrome, fungal

or=1.1 (indicates portal hypertension) - cardiac ascites, cirrhosis, Budd-Chiari syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Blood supply of the brain

A

Common carotids —> internal carotids —> opthalmic artery and then anterior and middle cerebral arteries
Subclavian arteries —> vertebral a. —> posterior inferior cerebellar a., then anterior spinal a., then basilar a. —> anterior inferior cerebellar a., then pontine a. —> superior cerebellar a., then posterior cerebral a. which connect to circle of willis vis posterior communicating a.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Middle cerebral artery supply

A

lateral surface of the frontal, parietal, and upper temporal lobes, genu and posterior limb of internal capsule, majority of the basal ganglia, proximal parts of the visual radiations as they emerge from the lateral geniculate nucleus of the thalamus and course in Meyer’s loop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Anterior cerebral artery supply

A

medial surface of the frontal and parietal lobes (motor and sensory areas for pelvis and lower limbs), superior inch of the frontal and parietal lobes, anterior 4/5 of corpus callosum, anterior limb of internal capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Posterior cerebral artery supply

A

inferior temporal lobe and occipital pole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Anterior cerebral artery occlusion deficits

A

spastic paresis and anesthesia of contralateral lower limb

Note: if bilateral, urinary incontinence can occur
- if anterior corpus callosum is involved, a transcortical apraxia of the left limbs may occur (disconnection of left hemisphere’s (language dominant) from motor cortex of right hemisphere)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Apraxia

A

Inability to perform particular purposive actions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Middle cerebral artery occlusion deficits

A
  • spastic paresis of the contralateral lower face and upper limb and anesthesia of the contralateral face and upper limb
  • Aphasia can occur when left MCA is affected and left-sided neglect can occur when right MCA is affected
  • Contralateral superior quadrantanopsia w/ occlusion of the branches supplying Meyer’s loop.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Vertebral a. course

A

through transverse processes of upper 6 cervical vertebrae; enters posterior fossa after passing through foramen magnum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Anterior spinal a. supply

A

ventrolateral 2/3 of cervical spinal cord and ventromedial part of medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

PICA supply

A

cerebellum and dorsolateral medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Labyrinthine a. supply

A

branch of the basilar a. that follows the course of CN VIII; supplies the inner ear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

AICA supply

A

part of pons, anterior and inferior cerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Superior cerebellar a. supply

A

rostral pons and superior cerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Pontine branches supply

A

pons via paramedian and circumferential branches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

PCA supply

A

midbrain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Midbrain CNs

A

III and IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Upper pons CNs

A

V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Lower pons CNs

A

VI, VII, VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Upper medulla CNs

A

IX, X, XII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Medial medullary syndrome

A

Occlusion of the vertebral a. or anterior spinal a.
Localizing sign
- CN XII - ipsilateral paralysis of half the tongue w/ atrophy (tongue deviates towards the lesion)
Affected nerve tracts
- medial lemniscus - contralateral deficit of proprioception and touch, pressure, and vibratory sensation in limbs and body
- pyramid (corticospinal tract) - contralateral spastic hemiparesis of both limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Lateral medullary syndrome (Wallenberg)

A

Occlusion of PICA
Localizing CNs
- vestibular or cochlear parts of CN VIII - may produce nystagmus, vertigo, N/V (w/ vestibular nystagmus, the fast component will be away from the side of the lesion)
*Lesions of the cochlear nucleus or auditory nerve produce an ipsilateral sensorineural hearing loss.
- CN IX - diminished or absent gag reflex
-CN X - dysphagia or hoarseness, palate will droop on affected side and the uvula will deviate away from the side of the lesion
- spinal nucleus and tract of CN V - loss of just pain and temperature on ipsilateral side of half the face (touch and corneal blink reflex will be intact)
Affected nerve tracts
- spinothalamic tracts - pain and temperature deficit in contralateral limbs and body
- descending hypothalamic fibers - ipsilateral Horner syndrome
* If solitary nucleus is affected, taste sensations may be altered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Medial Pontine Syndrome

A

occlusion of the paramedian branches of the basilar a.

  • CN VI - internal strabismus of the ipsilateral eye (diplopia on lateral gaze to the affected side)
  • Corticospinal tract - contralateral spastic hemiparesis of both limbs
  • Medial lemniscus may be affected - contralateral deficit of proprioception and touch pressure and vibratory sensations in the limbs and body.
  • CN VII may be affected if it extends laterally
  • Long tract signs are the same as in medial medullary syndrome but the CN signs localize the lesion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Upper motor neuron

A

Due to spinal cord lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Myesthenia gravis

A
  • AutoAbs against acetylcholine receptor on post-synaptic membrane
    Signs and symptoms:
  • extraocular muscle weakness (ptosis and diplopia), bulbar muscle weakness (jaw fatigue with chewing and dysarthria with talking).
  • symmetrical proximal weakness of the extremities (upper more than lower), neck (flexors and/or extensors), and bulbar muscles (dysarthria/dysphagia)
  • Normal reflexes, muscles bulk/tone, sensory function and autonomic function.

Diagnosis: CPK is normal differentiating it from primary muscle problem

  • Associated with the presence of a thymoma —> always order CT of the chest bc thymoma can sometimes be invasive.
  • Sometimes associated with thyroid disease —-> ultrasound can be helpful.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Amyotrophic lateral sclerosis

A
  • Affects distal muscles more

- sensory abnormalities and ocular deficits are usually absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Mononeuropathies

A
  • Affect both motor and sensory function of single nerve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Multiple sclerosis

A
  • Autoimmune CNS demylenating disease
  • Upper motor neuron signs
  • Oligoclonal IgG bands in the CSF with normal opening pressure, protein, and cell count.

Treatment of acute exacerbations:

  • IV steroids in symptoms are severe.
  • Mild sensory symptoms do not require steroids.
  • Steroids do not prevent future attacks or prevent progression.

Reduce frequency of acute exacerbations:
- interferon, plasmapheresis, cyclophosphamide, IV immunoglobulin, glatiramer acetate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Polyneuropathies

A
  • in diabetes mellitus
  • vitamin B12 deficiency
  • Guillain-Barre syndrome
  • Chronic inflammatory demyelinating polyneuropathy

Signs and symptoms: reduced or absent reflexes, parathesias, motor and sensory symptoms of both upper and lower extremities, but not usually bulbar symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Exertional heat stroke

A

Risk factors: obesity, certain medications (anticholinergics, antihistamines, phenothiazines, tricyclics)

Clinical manifestations: core temperature >104F AND CNS dysfunction (altered mental status, seizure, confusion, irritability)
- Additional organ or tissue damage (renal/hepatic failure, DIC, ARDS, coagulopathic bleeding)

Other possible signs and symptoms: dry or sweaty skin, hypotension, tachycardia, hyperventilation, diarrhea, cramps, ataxia
Management: rapid cooling: ice water immersion preferred, fluids, electrolyte correction, no role for antipyretic therapy

  • Evaporative cooling is preferred in nonexertional heat stroke (elderly patients with comorbidities).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Heat exhaustion

A

> 104 F, but no CNS dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Multiple system atrophy (Shy-drager syndrome)

A

Degenerative disease

Characteristics:

  • Parkonsonism
  • autonomic dysfunction
  • widespread neurological signs (cerbellar, pryamidal, LMN)
  • Accompanied by bulbar dysfunction and laryngal stridor.

Treatment: anti-Parkinsonism drugs are ineffective; treated w/ intavascular volume expansion w/ fludrocortisone, salt supplementation, alpha adrenergic agonists, and constrictive garments on the lower body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Idiopathic orthostatic hypotension

A
  • Degeneration of postganglionic sympathetic neurons

- Solely autonomic dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Familial dysautonomia (Riley-Day syndrome)

A

Autosomal recessive condition found in Ashkenazi Jews

- autonomic dysfunction with severe orthostatic hypotension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Chemotherapy-induced peripheral neuropathy

A
  • symmetrical parasthesias of the fingers and toes, early loss of ankle jerk reflexes, loss of pain and temperature sensation, occasional motor neuropathy
  • Commonly due to platinum-based meds (cisplatin), taxanes (paclitaxel), and vinca alkaloids (vincristine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Allodynia

A

Perception of a normally innocuous stimulus as painful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Benign essential tremor

A
  • action tremor
59
Q

Alzheimer’s disease

A

Pathophysiology: selective loss of cholinergic neurons

Early findings:

  • anterograde memory loss
  • visuospatial deficits
  • language difficulties
  • cognitive impairment with progressive decline

Late findings:

  • neuropsychiatric
  • dyspraxia (difficulty performing learned motor tasks)
  • lack of insight regarding deficits
  • noncognitive neurologic deficits (pyramidal and extra-pyramidal motor, myoclonus, and seizures)
  • urinary incontinence

Criteria:

  • two or more areas of cognitive deficits
  • progressively worsening memory and other cognitive function
  • no disturbance of consciousness
  • onset after 60
  • absence of other systemic or neurologic disorder causing progressive cognitive deficits

Treatment:

  • first-line: cholinesterase inhibitors (donepizil, galantamine, rivastigmine).
  • Moderate to severe: memantine
60
Q

Stroke due to endocarditis

A
  • commonly occurs in the MCA

- Antibiotics reduce the risk of septic emboli in patients with endocarditis.

61
Q

Guillain-Barre syndrome

A

associated with Campylobacter jejuni, Herpes viruses, Mycoplasma, and H. influenza as well as certain vaccines (influenza)

Cause: antibodies directed against Schwann cells

Clinical features: symmetric ascending muscle weakness with absent or depressed DTRs

  • bulbar symptoms (dysarthria and dysphagia)
  • Facial nerve palsy
  • Albumino-cytologic dissociation (elevated protein and normal cell count)

Diagnosis: nerve conduction studies which show demyelination

Treatment: IVIG or plasmapharesis
Miller-Fischer variant: begins with cranial nerve deficits (uncommon)

62
Q

Malignant hyperthermia

A

-affects genetically susceptible patients who have anesthesia with halothane or succinylcholine

63
Q

Seizures

A

Circumstances:

  • sleep loss
  • emotions
  • alcohol withdrawal
  • flashing light

Clinical clues:

  • aura
  • can occur with sleeping/sitting position
  • head movements
  • tongue biting
  • rapid, strong pulses

Sequelae:

  • delayed return to baseline
  • usually sleepy and confused afterward (postictal state)
64
Q

Syncope (vasovagal)

A

Circumstances:

  • upright position
  • emotions
  • heat
  • crowded places

Clinical cues:

  • symptoms of presyncope (lightheadedness)
  • unlikely to occur with sleeping/sitting position
  • rarely, several clonic jerks can occur with prolonged cerebral hypoperfusion as well as urinary incontinence
  • pallor and diaphoresis
  • weak, slow pulses

Sequelae:
- immediate spontaneous return

65
Q

Hypokalemia

A 
Symptoms:
- weakness
- fatigue
- muscle cramps
Severe:
- flaccid paralysis
- hyporeflexia
- tetany
- rhabdomyolysis
- arrhythmias

ECG findings:

  • broad flat T waves
  • U waves
  • ST depression
  • premature ventricular beats

Can lead to:

  • torsades de pointes
  • V fib
  • A fib
66
Q

Deep brain stimulation

A

Used to treat Parkinson’s disease, dystopia, or essential tremors; blocks faulty nerve signals that cause tremors, rigidity, etc.

67
Q

Lamotrigine

A

Lamictal

Used to treat bipolar I disorder and epilepsy (partial-onset seizures, generalized seizures of Lennox-Gastaut syndrome, and primary generalized tonic-clonic seizures)

Risk: serious skin rash - greater risk in pediatric pts

Metabolic inhibitor of OCT2

Mechanism: triazine derivative which inhibits the release of glutamate and inhibits voltage-sensitive Na channels, stabilizing neuronal membranes

  • weak inhibitor of 5-HT3 receptor
  • inhibits dihydrofolate reductase
68
Q

Lennox-Gastaut syndrome

A

Severe seizures in childhood

  • presentation usually before 8 yrs (typically 3-5)
  • may evolve from other epilepsy syndromes

Defining criteria:

  • multiple seizure types, particularly tonic and atypical absence seizures, but also atomic and myoclonic seizures. Periods of nonconvulsive status epilepticus occur in most cases at some stage.
  • slow (less than 2.5 Hertz) spike wave pattern on the interictal EEG that is generalized and usually has highest amplitude in the frontal region
  • mental retardation with or without other neurologic abnormalities.

Treatment:

  • no drug is highly effective
  • kerogenic diet and VNS
69
Q

Levetiracetam

A

Keppra

Use: myoclonic seizures (juvenile myoclonic epilepsy), partial-onset seizures, and primary generalized tonic-clonic seizures

Off-label: status epilepticus, in setting of subarachnoid hemorrhage to prevent seizures

Side-effects: high BP, behavioral problems,

Mechanism: unknown

70
Q

Donepizil

A

acetyl-cholinesterase inhibitor used to treat Alzheimer’s

71
Q

Pseudodementia

A
  • Key factor in differentiating between this and Alzheimers disease is the awareness of problems.
72
Q

Relapsing-remitting MS treatment

A

Interferon-beta slows the progression

73
Q

Progressive MS treatment

A

Methotrexate, cyclosporine, mitoxantrone

74
Q

Trigeminal neuralgia

A

Treatment of choice: carbamazepine (second-line treatment: gabapentin and lamotrigine)
- In cases resistent to medical therapy, treat with surgery to relieve pressure.

75
Q

Carotidynia

A
  • Inflammation of the carotids and the vagus

Diagnosis: clinical, but sometimes requiring MRI

76
Q

Burning mouth syndrome

A
  • caused by a virus

Symptoms and signs: reddened mucosa with significant pain
- aggravated by dryness

Treatment: supportive care

77
Q

Huntington’s chorea CT findings

A
  • atrophy of the caudate nucleus seen as enlargement of the lateral ventricles.
78
Q

Atrophy of the lenticular nucleus

A
  • seen in Wilson’s disease
79
Q

Pick’s disease

A

Ct findings: atrophy of the fronto-temporal cortex

80
Q

Agnosia

A
  • inability to recognize sensations and hence identify things.
81
Q

Creutzfeldt-Jakob disease

A 
Probable diagnosis:
- Rapidly progressive dementia
- 2 out of 4 clinical features:
   - myoclonus 
   - akinetic mutism
   - cerebellar or visual disturbance
   - pyramidal/extrapyramidal dysfunction (hypokinesia)
- Periodic sharp wave complexes on EEG (bi or tri-phasic)
           &/OR
- Positive 14-3-3 CSF assay

Definitive diagnosis includes above features in combination with
- brain biopsy findings (gold standard)
OR
- demonstrated PRNP gene mutations

  • Lack of inflammatory response
    Other symptoms: insomnia, apathy, behavioral changes, and impaired vision
82
Q

Normal pressure hydrocephalus

A

Additional symptoms: slow, broad-based, shuffling gait

  • Fecal incontinence may be seen in severe disease.
  • Memory loss w/o focal neurologic deficits

Diagnosis: Enlarged ventricles on CT or MRI along with normal opening pressure on LP

Treatment: sequential CSF removal (serial large volume LPs)
- Ventriculoperitoneal shunt may be placed if the patient responds to LP.

83
Q

Herpes encephalitis

A

Cause: most commonly HSV-1

Symptoms and signs: acute onset (

84
Q

Dominant optic atrophy

A

Kjer’s optic atrophy

Synopsis: affects the optic nerves, causing reduced visual acuity and blindness beginning in childhood

Clinical presentation:
2 forms:
1. Isolated bilateral optic neuropathy (non-syndromic)
2. Extra-ocular signs (syndromic)

Pathophysiology: optic nerve fiber loss due to mitochondrial dysfunction

Treatment: none

85
Q

Orthostatic tremor

A
  • Postural tremor thought to be a variant of essential tremor.
  • Occurs in the legs upon standing and is relieved by sitting down
  • High frequency (14-18 Hz) without other clinical symptoms.
86
Q

Large fiber peripheral neuropathy

A
  • Can present with action or postural tremors due to impaired proprioceptive input.
87
Q

Metastatic brain cancer

A

Lung > breast > unknown primary > melanoma > colon

Primarily solitary brain mets: breast, colon, renal cell carcinoma

Multiple brain mets: lung cancer, malignant melanoma

Rare brain mets: prostate cancer, esophageal, oropharyngeal, hepatocellular carcinoma, non-melanoma skin cancers

88
Q

Intracerebral hemorrhage

A

Characteristics: acute focal neurologic deficits that gradually worsen over time —> elevated intracranial pressure

Risk factor: hypertension

89
Q

Central cord syndrome

A

Cause: hyperextension injuries frequently in elderly patients with pre-existing degenerative changes in the C-spine

Mechanism: selective damage to the central portion of the anterior spinal cord, specifically the central corticospinal tracts and the decussating fibers of the lateral spinothalamic tract

Signs and symptoms: weakness more pronounced in the upper extremities
- May have loss of pain and temperature sensation in the arms due to damage to the spinothalamic tract

90
Q

Anterior (ventral) cord syndrome

A
  • Bilateral spastic motor paresis distal to the lesion

Cause: occlusion of the anterior spinal artery or burst fracture of the vertebra

91
Q

Brown-Sequard syndrome

A
  • Hemisection of the cord (most often due to a penetrating injury).

Characteristics:

  • Ipsilateral: weakness, spasticity, loss of vibration sense and proprioception
  • Contralateral: loss of pain and temperature sensation.
92
Q

Posterior (dorsal) cord syndrome

A
  • Bilateral loss of vibratory and proprioceptive sensation , often with weakness, parasthesias, and urinary incontinence or retention.

Causes: most commonly MS and vertebral artery dissection

93
Q

Primidone side effects

A
  • Is converted to phenylethylmalonamide and phenobarbital
  • Can participate acute intermittent porphyria: abdominal pain, neurologic and psychiatric abnormalities.
    diagnosis: test urine for porphobilinogen
94
Q

Parkinson’s disease

A

Treatment: amantadine (dopamine agonist)

95
Q

Hypopyon

A

Inflammatory cells in the anterior chamber of the eye

96
Q

Anterior spinal artery occlusion

A
  • Bilateral signs commonly seen at mid-thoracic levels with sparing of the dorsal columns.
  • Affects the corticospinal tracts and spinothalamic tracts —> spastic paresis and loss of pain and temperature.
97
Q

Miller-Fischer test

A
  • Assessment of gait and cognitive function both before and after a large-volume lumbar puncture to assess for normal pressure hydrocephalus
98
Q

Meniere’s disease

A

classic triad: episodes of dizziness lasting 30 minutes to several hours, unilateral tinnitus, and fluctuating hearing loss

-Thought to be due to an increase in the volume of endolymph —> permanent damage of the vestibular and cochlear appartuses

Treatment: symptomatic with meclizine and scopalimine

99
Q

Botulism

A
  • Descending motor weakness
100
Q

Allergic conjunctivitis

A

Treatment: frequent attacks - antihistamine and mast cell stabilizing properties (ketotifen - H1 antagonist , mast cell stabilizer and eosinophil inhibitor)

101
Q

Tenting at the junction of the optic nerve and the globe

A

Expanding of the retrobulbar space causing the globe to stretch the optic nerve

102
Q

Vitamin A deficiency

A

night blindness, xerosis and anemia

103
Q

Retinitis pigmentosa

A

progressive peripheral vision loss and night vision loss leading to central vision loss

Physical exam: mid-peripheral retinal hyperpigmentation and optic nerve waxy pallor

104
Q

Pseudotumor cerebri

A

Diagnosis:

1) MRI to r/o other intracranial processes
2) lumbar puncture to establish diagnosis
3) acetazolamide to treat

105
Q

Acute angle-closure glaucoma

A

Treatment: cholinergics, epinephrine, alpha-adrenergics,

emergency treatment: carbonic anhydrase inhibitors, mannitol, and topical beta-blockers

106
Q

Viral conjunctivitis

A

Symptoms: clear discharge, preauricular adenopathy

  • No treatment necessary, usually resolves in 5-7 days
107
Q

Progressive multifocal leukoencephalopathy

A

Symptoms: diplopia, gait ataxia, altered mental status

Diagnosis: CT scan of the brain showing diffuse lesions of the white matter

Treatment: initiate HAART therapy

108
Q

Central retinal artery occlusion

A
  • Sudden, painless unilateral loss of vision

Opthalmoscopy: pale retina and cherry red spot at the fovea

109
Q

Epidural abscess

A
  • Most commonly due to S. aureus, but also gram negative rods, Streptococci, and coagulase negative Staph.
110
Q

Periventricular leukomalacia

A

Leads to cerebral palsy, specifically spastic diplegia (more commonly of the lower extremities)

111
Q

Athetoid cerebral palsy

A

due to damage of the basal ganglia

Causes: kernicterus, asphyxia, or genetic/metabolic diseases

Symptoms: hypotonia with later rigidity and dystonic movements

112
Q

Cotard’s syndrome

A

Mental disorder in which patients complain of having lost their possessions, status, strength, and even inner organs

113
Q

Dementia pugilistica

A

post-traumatic dementia occurring after blunt-force trauma to the head

Symptoms: decreased attention, slowed information processing, increased distractibility, and problems with memory. Behavioral changes include impulsivity, depression, aggression, and personality changes

114
Q

beta-2 transferrin test

A

test to confirm leakage of CSF
- specific for CSF fluid, but can also be found in vitreous humor and the serum of newborns.

Signs of CSF leak: orthostatic headache and tinnitus, neck pain or stiffness, nausea and vomiting, anorexia, vertigo, dizziness, and change in vision

  • Defects in anterior cranial fossa —> leakage through the nose; defects in middle cranial fossa —> leakage through the ears

Complications: meningitis (most commonly with Strep pneumonae - most common cause of meningitis in adults)

115
Q

Reflex sympathetic dystrophy

A
  • Pain and swelling of one extremity (commonly a hand), associated with skin atrophy.
  • Thought to be due to vasomotor instability.
116
Q

Sebaceous cell carcinoma

A
  • Often mistaken for recurrent chalazion

- Diagnosed via biopsy

117
Q

Polycythemia vera

A

Treatment: phlebotomy along with hydroxyurea

  • Add in aspirin unless contraindicated.
  • Interferon A is used in patients who have refractory pruritis or don’t respond to other treatment.
118
Q

Anagrelide

A
  • Used to manage patients with thrombocytosis who are refractory to other forms of treatment.

Risks: heart failure and orthostatic hypotension in elderly with CV disease

119
Q

Chlorambucil

A
  • Used to treat CLL and non-hodgkin’s lymphoma
120
Q

Cluster headache

A
  • May be triggered by alcohol
  • Thought to be involve the hypothalamic nuclei that regulate circadian rhythm.
  • Pain and vasomotor symptoms probably mediated by seritogenic pathways
121
Q

Noncommunicating syringomyelia

A
  • Associated with trauma
122
Q

Syringobulbia

A

fluid-filled cavity in the medulla

Symptoms: dysphagia, nystagmus, phyrangeal and palatal weakness, asymmetric weakness and atrophy of the tongue, and loss of pain and temperature in the trigeminal nerve distribution.

123
Q

Non-proliferative diabetic retinopathy

A

small-vessel disease in the eye
- Occlusion, dilation and increased permeability of the small vessels in the eye —> microaneurysms
- Serous fluids and lipoproteins leak —> hard exudates
Small vessel ischemia —> microinfarctions of the nerve fiber layer —> cotton wool spots

124
Q

Macular edema treatment

A

lasar photocoagulation

125
Q

Proliferative diabetic retinopathy

A
  • Prolonged ischemia and neovascularization

Treatment: lasar photocoagulation to prevent blindness

126
Q

Cataracts

A
  • Followed closely until functional visual impairment results
  • Surgery removes the cataract, leaving the posterior lens capsule. if the capsule opacifies, it can be removed with laser (ultrasonic fragmentation of the lens nucleus).
127
Q

Bethanechol

A

Bladder-selective cholinergic agent that helps increase bladder contractility

128
Q

Oxybutinin

A

Anticholinergic used to treat urine loss

129
Q

Age-related macular exudative degeneration

A

Progression: age-related maculopathy (‘drussen’) —> atrophic (dry) or exudative (wet) degeneration —> no therapy has been proven to treat dry form, but lasar photocoagulation of the subretinal neovascular membranes may delay wet form

130
Q

CMV retinitis

A

Symptoms: scotoma, visual field deficits, floaters or flashing lights

Management: perform a fundoscopic exam to r/o retinal detachment —> treat with IV foscarnet or gancyclovir

131
Q

Acute dystonia

A
  • Includes torticollis
  • Can be due to drugs used to treat Parkinson’s disease (dopamine receptor blockade)

Treatment: dopamine agonst (carbidopa/levadopa), anticholinergic/antihistamine (diphenydramine, benztropine, trihexphenidyl), muscle relaxant or benzos
- Focal dystonias can be trated with botox

132
Q

Toxic labrynthitis

A

Vertigo caused by alcohol or medications (commonly aminoglycosides)

133
Q

Pronator drift

A

Sign of upper motor neuron problem - supination is weaker than pronation

134
Q

Mononeuritis multiplex

A

Painful, asymmetric, asynchronous sensory and motor peripheral neuropathy involving damage to > or = to 2 nerves

-Seen in patients with systemic vasculitides

135
Q

Cryoglobulinemia

A
  • Commonly seen in hepatitis B and C

Deposition of antibody-antigen complexes in small and medium sized arteries

Symptoms: palpable purpura, arthralgias, peripheral neuropathy, and hypocomplementemia

136
Q

corticosteroid-induced myopathy

A

-Lower extremity weakness and proximal muscle atrophy

Diagnosis: normal muscle enzymes and EMG results

Treatment: taper the steroids and wait for improvement (3-4 weeks)

137
Q

Type I spinal motor atrophy (Werdnig-Hoffman disease)

A

Degenerative disease of motor neurons that begins in fetal life and progresses during infancy
- Progressive denervation of muscles with following atrophy ; no DTRs with fasciculations of the tongue

  • Death occurs in early infancy to 2 years old

Diagnosis: muscle biopsy showing perineural denervation, or genetic tests

138
Q

Sumatriptan

A

serotonin agonist that is used to treat migraines

139
Q

Hypoxic-ischemic encephalopathy

A
  • most common cause of neonatal seizures

Treatment: benzos

140
Q

Tuberous sclerosis

A

Symptoms: hypopigmented ash-leaf lesions (more visible under UV light), infantile spasms and seizures —> mental retardation

Cause: seizures are thought to be caused by excess CRH which causes excess excitability

Diagnosis: EEG showing hypsarrhythmia (high voltage, asynchronous chaotic slow wave activity)

Treatment: ACTH which suppresses CRH

141
Q

Wernicke’s encephalopathy

A

Cause: thiamine deficiency

Classic triad:

  1. encephalopathy w/ disorientation and indifference
  2. oculomotor dysfunction (nystagmus, lateral rectus plasy and conjugate gaze palsies)
  3. Gait ataxia due to combined polyneuropathy, cerebellar involvement, and vestibular paresis

Treatment: give magnesium, thiamine and glucose

  • magnesium is needed for thiamine transport into neurons
  • give thiamine before glucose because glucose will use up pyruvate dehydrogenase for which thiamine is a cofactor, making the problem worse
142
Q

Delerium tremens

A

Treatment: benzodiazipines and haloperidol (for agitation)

143
Q

Carotid artery dissection signs

A

Horner’s syndrome: miosis, anhydrosis, and ptosis

Internal Medicine (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions