Brainscape's Knowledge GenomeTM

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


See full index

Step 2 > Neuro 1 > Flashcards

Neuro 1 Flashcards

1
Q

What is the most common primary brain malignancy?

A

Glioblastoma (aka grade IV astrocytoma, formerly glioblastoma multiforme)

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

Classic CT/MRI findings in glioblastoma?

A

Butterfly appearance with central necrosis (typical of glioblastoma); heterogenous serpiginous contrast enhancement (typical of high-grade astrocytoma)

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

Patients with brain metastases usually have a duration of symptoms of…?

A

Less than 2 months

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

General site of metastasis in patients with brain mets?

A

Gray-white junction or watershed zones

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

What is the most common cause of spontaneous lobar hemorrhage?

A

Cerebral amyloid angiopathy (especially in adults >60)

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

What causes cerebral amyloid angiopathy?

A

Beta-amyloid deposition in the walls of small- to medium-size cerebral arteries, resulting in vessel wall weakening and predisposition to rupture

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

What is the most common cause of intracranial hemorrhage in children?

A

AV malformation rupture

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

What causes a subdural hematoma and what are some risk factors?

A

Rupture of bridging veins, most commonly from head trauma; advanced age, chronic alcoholism, anticoagulant use

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

How does subdural hematoma appear on non-contrast head CT?

A

Crescent-shaped hyperdensity that crosses suture lines

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

How does ischemic stroke appear on CT scan?

A

Area of hypodensity affecting a vascular distribution

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

What causes an epidural hematoma?

A

Meningeal artery tears, typically due to traumatic head injury

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

How does an epidural hematoma appear on non-contrast head CT?

A

Biconvex hyperdensity that does NOT cross suture lines

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

What causes subarachnoid hemorrhage and how does it present?

A

Ruptured saccular (berry) aneurysms; abrupt onset of severe (thunderclap) headache; focal neuro deficits are uncommon

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

How does subarachnoid hemorrhage appear on CT?

A

Hyperattenuation of the sulci and basal cisterns on head CT

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

Presentation - sudden impairment of consciousness in children age 4-10 without loss of postural tone, occur throughout the day without warning, short (<20 seconds), may be accompanied by simple automatisms (eyelid fluttering, lip smacking, etc.)

A

Absence seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Absence seizures can usually be provoked by ___.

A

Hyperventilation

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

Dx absence seizures?

A

EEG - 3-Hz spike-wave discharge pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

First-line Rx for absence seizures?

A

Ethosuximide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Age of presentation of myasthenia gravis in men and women?

A

Women - 2nd to 3rd decade

Men - 6th to 8th decade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Presentation of myasthenia gravis?

A

Fluctuating and fatigable proximal muscle weakness worse later in the day

  • Ocular (eg, diplopia, ptosis)
  • Bulbar (eg, dysphagia, dysarthria)
  • Respiratory muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

List 4 general causes of myasthenia gravis exacerbations.

A
  1. Medications
  2. Pregnancy/childbirth
  3. Surgery (especially thymectomy)
  4. Infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

List 5 classes of medications that can cause myasthenia gravis exacerbations.

A
  1. ABX (FQs, AGs)
  2. Anesthetics (neuromuscular blocking agents)
  3. Cardiac medications (beta blockers, procainamide)
  4. Other (mag sulfate, pencillamine)
  5. Tapering immunosuppressive medications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What causes MG?

A

Autoantibody-mediated degradation of ACh receptors at the NMJ

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

How does the ice pack test support the diagnosis of MG?

A

Ice pack applied over the eyelids for several minutes leads to improved ptosis; cold temperature improves muscle strength by inhibiting the breakdown of ACh at the NMJ, increasing availability

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

If the ice pack test is positive, what should be done next?

A

Confirmatory testing with ACh receptor Ab (highly specific)

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

Disruption of the oculosympathetic chain causes ___.

A

Horner syndrome

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

Presentation of Horner syndrome?

A

Ipsilateral ptosis, miosis, anhidrosis

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

What causes Lambert-Eaton myasthenic syndrome?

A

Autoantibodies directed against presynaptic calcium channels in the NMJ, leading to impaired ACh release

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

Presentation of Lambert-Eaton myasthenic syndrome?

A

Slowly progressive proximal muscle weakness and depressed deep tendon reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Presentation of oculomotor nerve palsy?

A

Mydriasis, ptosis, down-and-out deviation of the eye

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

Causes of oculomotor nerve palsy?

A

Nerve compression (due to posterior communicating artery aneurysm or an uncal herniation)

Microvascular nerve ischemia (due to DM)

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

Cause of Guillain-Barre syndrome?

A

Immune-mediated demylinating polyneuropathy

Preceding GI (Campylorbacter) or respiratory infection

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

Presentation of GBS?

A 
Parasthesia, neuropathic pain
Symmetric, ascending weakness
Decreased/absent DTRs (areflexia)
Autonomic dysfunction
Respiratory compromise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Dx GBS?

A

Clinical
Supportive findings:
-CSF: increased protein, normal leukocytes
-Abnormal EMG and nerve conduction

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

Management of GBS?

A

Monitor autonomic and respiratory function

IVIG or plasmaphresis

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

Once Guillan Barre Syndrome is suspected in a hemodynamically stable patient, what is the next step in management?

A

Assess pulmonary function with spirometry
-FVC and negative inspiratory force monitor respiratory muscle strength; serial testing should be performed given the potential for rapid progression

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

What finding on PFTs indicates impending respiratory failure warranting endotracheal intubation? What are other indications for elective or emergency intubation?

A

Decline in FVC to 20 or less mL/kg; respiratory distress, severe dysautonomia, widened pulse pressure

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

What is the most common neoplasm to metastasize to the brain? List the next 4 most common.

A

Lung > Breast > Unknown primary > Melanoma > Colon

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

Presentation of brain mets on MRI?

A

Multiple, well-circumscribed lesions with vasogenic edema at the grey and white matter junction

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

List the 3 cancers that cause primarily solitary brain mets.

A

Breast
Colon
Renal cell carcinoma

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

List the 2 cancers that cause multiple brain mets.

A

Lung cancer

Malignant melanoma

42
Q

List 5 cancers that rarely cause brain mets.

A 
Prostate
Esophageal
Oropharyngeal
HCC
Non-melanoma skin cancers
43
Q

Lacunar infarctions are most typically seen in patients with ___.

A

Systemic hypertension

44
Q

List the 4 benign sellar masses.

A

Pituitary adenoma (most common)
Craniopharyngioma
Meningioma
Ptiucytoma (low-grade glioma)

(May also be malignant - primary or metastatic)

45
Q

Craniopharyngiomas are benign tumors arising from ___ and most commonly occur in what age group?

A

Rathke’s pouch; children. However, nearly 50% occur in those age >20, especially between 55-65

46
Q

2 types of cerebellopontine angle tumors?

A

Acoustic neuromas; meningiomas

47
Q

Symptoms of cerebellopontine angle tumors?

A

Headache, hearing loss, vertigo, tinnitus, balance problems; do not usually cause visual disturbances, as they are below the optic pathways

48
Q

Presentation - tunnel vision

A

Open-angle gluacoma

49
Q

Presentation - acute to subacute painful vision loss with abnormal pupillary response to light in the affected eye

A

Optic neuritis

50
Q

Presentation - headache, transient visual symptoms, pulsatile tinnitus; papilledema, visual field loss, CN 6 palsy

A

Pseudotumor cerebri

51
Q

Features suggestive of psychogenic non-epileptic seizure (PNES)?

A

Forced eye closure, side-to-side head or body movements, memory recall of the event, lack of post-ictal confusion

52
Q

Neurofibromatosis type 1 (NF1) is an autosomal ___ neurocutaneous disorder associated with what findings?

A

Dominant; cafe-au-lait macules, axillary and inguinal freckling, increased risk of seizures, learning disabilities, optic pathway gliomas, Lisch nodules, neurofibromas, pseudoarthrosis, scoliosis

53
Q

List the 3 major types of headaches.

A
  1. Migraine
  2. Cluster
  3. Tension
54
Q

Compare the sex predilection among the three major types of headaches.

A
  1. Migraine - F>M
  2. Cluster - M>F
  3. Tension - F>M
55
Q

Compare the presence of family history among the three major types of headaches.

A
  1. Migraine - often present
  2. Cluster - no
  3. Tension - no
56
Q

Compare the onset among the three major types of headaches.

A
  1. Migraine - variable
  2. Cluster - during sleep
  3. Tension - under stress
57
Q

Compare the location of the three major types of headaches.

A
  1. Migraine - often unilateral
  2. Cluster - behind one eye
  3. Tension - band-like pattern around the head (bilateral)
58
Q

Compare the character of the three major types of headaches.

A
  1. Migraine - pulsatile and throbbing
  2. Cluster - excruciating, sharp and steady
  3. Dull, tight, and persistent
59
Q

Compare the duration of the three major types of headaches.

A
  1. Migraine - 4-72 hours
  2. Cluster - 15-90 minutes
  3. Tension - 30 minutes to 7 days
60
Q

Compare the associated symptoms of the three major types of headaches.

A
  1. Migraine - auras, photophobia and phonophobia, and nausea
  2. Cluster - sweating, facial flushing, nasal congestion, lacrimation, and pupillary changes
  3. Tension - muscle tenderness in the head, neck, or shoulders
61
Q

How should tension-type headaches be managed (intermittent vs. more frequent)?

A

If intermittent (no more than 1 day/month), can use analgesics +/- caffeine without concern for developing medication overuse headache

If more frequent, longer, or disabling, consider prophylactic medication (eg, amitriptyline) as well as CBT for stress-reduction

62
Q

Presentation - progressive morning headache associated with frequent N/V, +/- seizure or neurological deficits

A

Brain tumors

63
Q

Presentation - unilateral recurrent periorbital pain that resolves and recurs with associated ipsilateral miosis and ptosis

A

Cluster headaches

64
Q

Presentation - patients >50, new-onset headaches localized to the temples, may be associated with fever, weight loss, vision changes, and jaw claudication

A

Giant cell arteritis

65
Q

DDx - neuromuscular weakness - general locations of lesion?

A
  1. UMNs
  2. Anterior horn cells
  3. Peripheral nerves
  4. NMJ
  5. Muscle fibers
66
Q

DDx - neuromuscular weakness due to an UMN lesion?

A
  1. Leukodystrophies
  2. Vasculitis
  3. Brain mass
  4. Vitamin B12 deficiency
67
Q

DDx - neuromuscular weakness due to anterior horn cell lesions?

A
  1. Spinal muscular atrophy (flaccid paralysis in infancy)
  2. ALS
  3. Paraneoplastic syndromes
  4. Poliomyelitis
68
Q

DDx - neuromuscular weakness due to peripheral nerve lesions?

A
  1. Hereditary primary motor sensory neuropathy
  2. GBS
  3. Diabetic neuropathy
  4. Amyloid neuropathy (myeloma)
  5. Lead poisoning
69
Q

DDx - neuromuscular weakness due to NMJ lesion?

A
  1. MG (weakness worse with use, better with rest)
  2. Lambert-Eaton (progressive proximal muscle weakness)
  3. Organophosphate poisoning (weakness + multisystem cholinergic symptoms)
  4. Botulism (descending paralysis)
70
Q

DDx - neuromuscular weakness due to muscle fiber lesion?

A
  1. Muscular dystrophies
  2. Polymyositis and dermatomyositis
  3. Hypothyroidism
  4. Corticosteroids
  5. HIV myopathy
71
Q

What is the pathogenesis of GBS?

A

Immune-mediated polyneuropathy caused by demyelination of peripheral nerve fibers; most patients have a preceding respiratory or GI infection that triggers an immune response. Antibodies are then redirected toward cross-reacting antigens on myelin or axons (molecular mimicry)

72
Q

Presentation of GBS?

A

Ascending weakness, often accompanied by paresthesias and neuropathic pain; most severe symptoms include flaccid paralysis with diminished or absent DTRs and respiratory failure. Accompanying autonomic symptoms (BP/HR instability, ileus, etc.) often parallel the severity of motor deficits

73
Q

Rx GBS?

A

IVIG or plasmapheresis

74
Q

What is autonomic dysreflexia?

A

Complication of spinal cord injury above T6; in an intact spinal cord, sympathetic activity is modulated by higher-level neurons. SCI results in loss of modulatory activity below the lesion. Noxious stimuli (eg, urinary retention, constipation, pressure ulcers) can cause an unregulated sympathetic response, leading to vasoconstriction and severe hypertension. Above the lesion, a compensatory parasympathetic response causes diaphoresis, flushing, bradycardia, and nasal congestion. Vasodilation occurs but cannot overcome the sympathetic drive to normalize systemic pressure.

75
Q

Complications of autonomic dysreflexia?

A

Intracranial hemorrhage or progressive bradycardia with cardiac arrest

76
Q

Management of autonomic dysreflexia?

A

Close monitoring of blood pressure; place the patient in an upright position to encourage orthostatic BP reduction

Search for precipitating events (urinary retention, fecal impaction, pressure sores)

Remove tight-fitting close

Short-duration antihypertensives may be needed

77
Q

What is carotid sinus hypersensitivity and how does it typically present?

A

Significant drop in heart rate (pauses) and blood pressure (>50 mm Hg) following carotid massage; lightheadedness or syncope after carotid manipulation in older patients with atherosclerotic disease

78
Q

Presentation - older individual, back/shoulder pain following physical activity, loss of shoulder abduction strength, reduced sensation in the left lateral forearm

A

C5-C6 nerve root impingement from cervical radiculopathy; may be due to acute cervical disc herniation or cervical spondylosis

79
Q

What are the two clinical syndromes associated with cervical spondylosis?

A
  1. Cervical radiculopathy

2. Compressive cervical myelopathy

80
Q

What causes cervical radiculopatyh and how does it present?

A

Degeneration and osteophyte formation in the zygapophyseal and uncovertebral joints -> intervertebral foramen narrowing and compressive nerve root symptoms (progressive neck, shoulder, and/or arm pain plus weakness in a myotome and sensory loss in a dermatome)

81
Q

What causes compressive cervical myelopathy and how does it present?

A

Degeneration and thickening of the lateral vertebral bodies and posterior longitudinal ligament lead to spinal canal narrowing and subsequent spinal cord compression; neck pain, LMN signs in the upper extremities, UMN signs in the lower extremities, and bowel/bladder dysfunction

82
Q

First test of choice in the setting of cervical radiculopathy?

A

MRI of cervical spine

83
Q

Presentation of diabetic neuropathy?

A

Alterations in sensation, including loss of proprioception; motor findings may be a late manifestation in the most severe cases

84
Q

Why can uncontrolled infection of the skin, sinuses, and orbit spread to the cavernous sinus?

A

Because the facial/ophthalmic venous system is valveless

85
Q

Presentation of cavernous sinus thrombosis?

A

Intracranial HTN -> headache, vomiting, papilledema; followed by low-grade and periorbital edema several days later (due to impaired venous flow); CN lesions may include binocular palsies, periorbital edema, hypoesthesia, or hyperesthesia in V1/V2 distribution (unilateral -> bilateral)

86
Q

What are the structures surrounding the cavernous sinus?

A

Optic chiasm
Internal carotid artery with PCA branch
Pituitary gland
CN III, IV, V (1 and 2), VI

87
Q

Imaging modality of choice to diagnose cavernous sinus thrombosis?

A

MRI with MR venography

88
Q

Rx cavernous sinus thrombosis?

A

Broad-spectrum IV ABX, prevention or reversal of cerebral herniation

89
Q

___ should be considered in any patient with fever, headache, and focal findings on neurologic examination.

A

Brain abscess

90
Q

Inheritance pattern of neurofibromatosis type 1?

A

Autosomal dominant

91
Q

Clinical features of NF1?

A

Multipel cafe-au-lait macules, axillary and inguinal freckling, Lisch nodules (iris hamartomas) neurofibromas, learning disability, scoliosis, pseudoarthritis

Increased risk of neurological disorders and intracranial neoplasms (optic pathway glioma)

92
Q

What type of tumor typically develops in patients with neurofibromatosis type 2?

A

Bilateral acoustic neuromas (aka vestibular schwannomas)

93
Q

Clinical features of tuberous sclerosis?

A

Benign tumors in multiple organs -> ash leaf spots, angiofibroms, shagreen patches, intracardiac rhabdomyomas

94
Q

Clinical features of fragile X syndrome?

A

Intellectual disability, large ears, long/narrow face, macroorchidism, seizures

95
Q

Clinical features of Sturge-Weber syndrome?

A

Port-wine stain on the face
Ocular disease (visual deficits, glaucoma, etc.)
Leptomeningeal capillary-venous malformation (may cause seizures)

96
Q

Presentation - areflexic weakness in the upper extremities and dissociated sensory loss in a cape distribution

A

Syringomyelia

97
Q

What is syringomyelia and what is the most common cause?

A

Fluid-filled cavity within the cervical and thoracic spinal cord that is most commonly associated with Arnold Chiari malformation type 1

98
Q

Describe the pathogenesis of syringomyelia.

A

Lesion disturbs the decussating STTs in the anterior commissure; vibration/proprioception is preserved as the dorsal spinal column is not usually affected (dissociated sensory loss). As the cavity enlarges, there can be interruption of the anterior horn gray matter, resulting in LMN signs in the upper limbs (areflexic weakness)

99
Q

Presentation - sudden flaccid paralysis, loss of pain and temperature below the lesion; intact position, vibration, touch

A

Anterior cord syndrome

100
Q

Presentation - sub-acute onset of flaccid paralysis and loss of all types of sensation below the level of the lesion

A

Segmental demyelination/inflammation of the spinal cord (transverse myelitis)

Step 2 (27 decks)

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