Neuro - Esper Flashcards

1
Q

Clinical features and diagnostic tests for Creutzfeldt - Jakob disease

A
  • CSF: 14-3-3 protein
  • MRI: high signal intensity in the caudate nucleus and putamen bilaterally on T2
  • EEG: characteristic bi- or triphasic spike wave complexes
  • Patient presentation: rapidly progressing dementia and myoclonus
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2
Q

different peripheral nerve manifestations of diabetes

A
  • Mononeuropathy (a single nerve) & Mononeuropathy Multiplex
  • Symmetric Sensorimotor Neuropathy. The classic “glove and stocking” neuropathy
  • Autonomic: GI and GU symptoms, impotence, and impaired sweating and vascular function
  • Thoracoabdominal Radiculopathy
  • Amyotrophy: Gradually progressive proximal leg weakness, Painful with NO sensory loss
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3
Q

Which nerves are lost first in diabetic neuropathy?

A

Small fibers (burning, tingling, numbness, pain) are lost first followed by large fibers (weakness, vibratory and position sense, numbness, areflexia)

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4
Q

Diagnostic tests for Polymyositis

A

Antinuclear antibody assay: positive in one third of patients with Polymyositis
MRI and ultrasonography: will show abnormalities due to inflammation of muscles

Biopsy: will show evidence of inflammation

Labs: serum creatinine and creatine kinase are commonly increased.

Signs and symptoms include: Symmetrical proximal muscle weakness, aches and cramping, morning stiffness, fatigue, anorexia, fever, weight loss, arrhythmias, dyspnea, dysphagia, aspiration, constipation, and reflux.

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5
Q

A manifestation that is due to the presence of a neoplasm or cancer, however, it is not caused by the local presence of the cancer. When the body mounts an immune response against a tumor, sometimes the antibodies that are formed recognize antigens that are similar to those present elsewhere in the body on healthy tissues. Because of this, these antibodies target the healthy tissues and cause damage to them.

A

Paraneoplastic syndromes

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6
Q

Lambert-Eaton Syndrome

A

most commonly due to small cell carcinoma of the lung, where antibodies are formed against presynaptic calcium channels of the neuromuscular junction

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7
Q

Proximal muscle weakness that improves with use. Dry mouth, pupils may not be reactive. No improvement of symptoms with use of anticholinesterase use. Often resolves with the resection of the tumor (commonly a thymoma)

A

Lambert-Eaton Syndrome clinical findings

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8
Q

Elevated intracranial pressure, headache, papilledema, and CN VI palsy. Spinal tap pressure (>250 mm H2O), MRI

A

Pseudotumor cerebri

Treatment: Self-limiting, diuretics, surgery (shunting)

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9
Q
  • Straw colored/non-purulent CSF
  • Increased lymphocytes
  • Mildly elevated protein concentration
  • Normal glucose concentration
A

Viral Infection

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10
Q

What signs do patients have to present with for Wernicke Encephalitis

A

Caine criteria for diagnosis in which patients must present with two of the following four signs: Thiamine dietary deficiency, oculomotor abnormalities, cerebellar dysfunction, either altered mental status or mild memory impairment. The Caine criteria are considered more sensitive for making a diagnosis.

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11
Q

Describe the diagnostic tests and signs and symptoms of Lyme disease

A

Localized: Bull’s eye rash (painless) lasting 1-30 days
Early Disseminated: meningitis, carditis, radiculoneuropathy, cranial neuropathy lasting weeks to months.
Late Disseminated: persistent arthritis and encephalopathy

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12
Q
  1. Explain common symptoms and signs of Myasthenia Gravis
A

Fluctuating weakness affecting facial and pharyngeal muscles, respiratory failure, aspiration, and muscle wasting in 10% of patients. Symptoms are better in the morning and get worse as the day progresses. The disease is usually associated with a thymoma. There are ocular and generalized forms (ocular symptoms in 40% initially and eventually appear in 85%).
Flu shots aggravate MG.

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13
Q

Treatment of Myasthenia Gravis

A

Pyridostigmine is used to treat MG.

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14
Q

Clinical presentation and treatment of cluster headaches

A

Cluster headaches are generally found more in men over 19 yo. There will be multiple attacks per day/week lasting 15mins - 3 hrs. Intensity is severe and unilateral in the supraorbital/temporal region. There is no aura but patients can have lacrimation and rhinorrhea. This often occurs at night and can lead to suicide.

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15
Q

Treament of cluster headaches

A
if symptomatic, 
Oxygen
Dihydroergotamine
Sumatriptan
Sphenopalatine block
Intranasal lidocaine
Intranasal capsaicin
Indomethacin
Opioids
for prophylaxis.
Verapamil
Steroids
Lithium
Methysergide
Valproic acid
Neuroleptics
Clonidine
Daily triptans or ergots
Daily opioids
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16
Q

Adrenoleukodystrophy

A

X-linked inherited disorder causing atrophy of the adrenal cortex and demyelination of the nervous system. This increases levels of very long chain fatty acids. Affects kids 4-8 years old.

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17
Q

Metachromatic leukodystrophy

A

Autosomal recessive caused by a defect in Arylsufatase A resulting in the accumulation of sulfatides causing myelin breakdown. Macrophages containing sulfatides bind to certain types of dyes, which change absorbance spectrum.

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18
Q

Alexander disease

A

Rare neurological disease in infants and kids which involves loss of myelin in the brain and accumulation of irregular extracellular fibers (AKA Rosenthal fibers)

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19
Q

Krabbe disease

A

Deficiency of Galactocerebroside Beta Galactosidase. Autosomal recessive

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20
Q

Demyelinating disease most commonly show white matter changes on MRI:

A
  • CADASIL: Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy. Mutation of Notch 3 gene on Chromosome 19. It’s associated with migraines.
  • Multiple Sclerosis
  • Marchiafava-Bignami: affects corpus callosum and anterior commissure. Most common patients are men with alcoholism
  • Wernicke-Korsakoff
  • Mercury Poisoning
  • Subacute Combined Degeneration
  • Progressive Multifocal Dystrophy (from JC virus)
  • Neuromyelitis Optica: variant of MS also called Devic disease. Worse than MS and happens more in the Asian population
  • Subacute Sclerosing Panencephalitis
  • Acute Disseminated Encephalomyelitis: follows viral infection or viral immunization. Headache, lethargy, and coma occur and are more common than focal findings
  • Central Pontine Myelinolysis: due to rapid correction of hyponatremia. This causes rapidly developing quadriplegia. Associated with alcoholics.
21
Q

etiology and diagnosis of an acute ischemic stroke versus a hemorrhagic stroke

A

On CT a hemorrhagic stroke would show immediately. However, CT scanning is insensitive for small or early ischemic infarcts. Diffuse Weighted Imaging MRI can more accurately identify areas of ischemia within minutes of onset.

22
Q

clinical and laboratory findings in B12 deficiency

A

B12 deficiency will cause pernicious anemia and sometimes Subacute Combined Degeneration. Signs and symptoms include:
• Myelin loss in the posterior columns causing sensory ataxia, paresthesias in the feet, impaired vibration and position sense, spasticity, hyperreflexia, and Babinski sign.
• Increased levels of Homocysteine and Methylmalonic acid levels

23
Q

clinical features of and diagnostic tests used in HSV Encephalitis

A

HSV encephalitis is caused by HSV-1 that enters the brain via the trigeminal ganglion or olfactory bulbs hence predilection for the temporal and frontal lobes.
Signs and symptoms include: fever, headache, focal seizures, focal signs (aphasia, personality changes, agitation, hallucinations), meningeal signs, and déjà vu phenomenon.
Diagnosis: CSF (increased white cells, red cells and protein; decreased or normal glucose), CSF PCR for HSV, EEG, imaging, and brain biopsy.

24
Q

Differentiate Guillain-Barré and chronic inflammatory demyelinating polyradiculoneuropathy

A

CIDP produces manifestations similar to GBS but symptoms tend to come on more slowly and progress for a longer period of time (namely, CIPD lasts longer than 8 weeks).

25
Q

clinical findings, diagnostic tests and treatment for multiple sclerosis

A
  • Motor: weakness, spasticity, UMN (hyperreflexia, Babinski), fatigue
  • Sensory: Vibratory, pain, temperature, and crude touch loss
  • Lhermitte Sign: electrical sensation down the back after flexion of the neck
  • Optic neuritis: painful loss of vision
  • CN problems: facial pain, numbness for any of the CN
  • Internuclear Ophthalmoplegia
  • Cerebellar ataxia (gait, tremor)
  • Autonomic Dysfunction: Bowel (constipation), Bladder problems, Sexual Dysfunction
  • Psychiatric: depression, bipolar disorder, cognitive disorder, memory trouble
  • Symptoms may be worsened or precipitated by Uhtoff’s phenomenon (exposure to heat)

Diagnosis:
• MRI of brain & spinal cord: look for abnormal lesions of the white matter (look for 2 or more lesions at 1 period of time)
• CSF evaluation looking for Oligoclonal Bodies
• Evoked potentials: visual (optic nerve), brainstem auditory (pontine lesions), and somatosensory (spinal cord)
• History & Physical

Treatment:
• Solumedrol: steroid that is used to treat relapses.
• Usually treated with disease modifying therapies and symptomatic therapies:
• Interferon Drugs, Glatiramer acetate, Natalizumab, Fingolimod, Mitoxantrone, Teriflunomide, and Dimethyl fumarate

26
Q
  1. Describe the clinical presentations, diagnosis and treatment of Alzheimer Disease
A

Clinical findings: most common dementia over age 65. Progressive, degenerative brain disease characterized by memory impairment/dementia early on, and changes in behavior, personality, judgment and ADLs. Risk factors include Down syndrome, family history, and advanced age. Geographic or temporal disorientation, day-night disorientation, language deterioration, wandering, irritability, depression, hallucinations, delusions, agitation, incontinence, and total dependence on caregivers are also common.

Diagnosis: clinical criteria, mental status exam, and physical and neurological exams. Upon death, histopathological study shows extracellular deposition of Amyloid Beta Protein, intracellular Neurofibrillary Tangles, and loss of neurons, especially in the hippocampus.

Treatment:
Cholinesterase Inhibitors: Donepezil, Rivastigmine, Galantamine, and Tacrine.
NMDA receptor antagonist: Memantine
Patient education: drugs won’t cure; only reduce symptoms, give patients simple instructions, react calmly, and avoid confrontation.

27
Q

CSF: 14-3-3 protein

A

Creutzfeldt - Jakob disease

28
Q

EEG: characteristic bi- or triphasic spike wave complexes

A

Creutzfeldt - Jakob disease

29
Q

Patient presentation: rapidly progressing dementia and myoclonus

A

Creutzfeldt - Jakob disease

30
Q

Patient presents with Symmetrical proximal muscle weakness, aches and cramping, morning stiffness, fatigue, anorexia, fever, weight loss, arrhythmias, dyspnea, dysphagia, aspiration, constipation, and reflux. Labs: serum creatinine and creatine kinase are commonly increased.

A

Polymyositis

31
Q

Treatment for pseudotumor cerebri

A

Treatment: Self-limiting, diuretics, surgery (shunting)

32
Q
  • Cloudy/purulent CSF
  • Increased neutrophils/PMNs
  • Increased protein concentration
  • Decreased glucose concentration
A

Bacterial infection

33
Q

Demyelination due to B12 deficiency commonly affects the posterior columns. Signs include ataxia, muscle weakness, and incontinence.

A

Subacute combined demyelination Syndrome

34
Q

Degeneration of peripheral nerve axons due to malnourishment and/or excessive ethanol levels. It’s usually symmetric and predominantly distal. Signs include paresthesia, muscle weakness, and ataxia.

A

Alcoholic polyneuropathy

35
Q

Demyelination of corpus callosum and adjacent structures due to chronic alcohol use. Signs include cognitive impairment (dementia), ataxia, apraxia, urinary incontinence, and seizures (possibly).

A

Marchiafava-Bignami

36
Q

Due to thiamine deficiency. Wernicke: encephalopathy, oculomotor dysfunction, gait ataxia. Korsakoff: late sequelae of Wernicke with anterograde and retrograde amnesia with confabulation

A

Wernicke-Korsakoff syndrome

37
Q

Encephalopathy, oculomotor dysfunction, gait ataxia

A

Wernicke Encephalitis

38
Q

Treatment for Wernicke Encephalitis

A

Treatment: thiamine (before glucose), stop drinking alcohol, improve diet

39
Q

Differentiate between folate and B12 deficiency using homocysteine and Methylmalonic acid

A

Vitamin B12 deficiency causes both hyperhomocysteinemia and increase Methylmalonic acid.

A folate deficiency will just be homocysteine

40
Q

CSF increased white cells, red cells and protein; decreased or normal glucose,

A

HSV Encephalitis

41
Q

How quickly is the onset of Guillaine-Barre?

A

Very rapid

42
Q

Motor weakness, spasticity, UMN signs(hyperreflexia, Babinski), fatigue. Vibratory, pain, temperature, and crude touch loss. Painful loss of vision. Internuclear Ophthalmoplegia. Bowel (constipation), Bladder problems, Sexual Dysfunction .

A

Multiple sclerosis

43
Q

MRI shows lesions of brain & spinal cord along the ventricles. CSF evaluation looking for Oligoclonal Bodies

A

Multiple sclerosis

44
Q

Treatment for Multiple sclerosis

A

“So interferon, Glad Natalie forgot Mitch’s Terimusu, he’s Dad’s Fumming”

Solumedrol: steroid that is used to treat relapses.
• Usually treated with disease modifying therapies and symptomatic therapies:
• Interferon Drugs, Glatiramer acetate, Natalizumab, Fingolimod, Mitoxantrone, Teriflunomide, and Dimethyl fumarate

45
Q

Patient presents with painful side around the left side of his umbilicus. He notices it seem to wrap around towards the back side and is in just one area. On physical examination you notice there are no vesicles of eruptions. Patient mentions recent weight loss and is diabetic. What is the Dx?

A

Diabetic Thoracoabdominal Radiculopathy. Damage to the root

46
Q

Features of Gullaine Barre

A
Ascending paralysis
Areflexia
Loss of propioception
No affect on EOM
Pain
47
Q

Features of Chronic Inflammatory Demyelinating polyneuropathy

A

Duration of symptoms to be greater than 8 weeks for the diagnosis of CIDP to be made.

Weakness
Areflexia
Pain
numbness, tingling

48
Q

When do you treat prophylactically for headaches

A

Twice weekly or less - acute

Daily or every other day - prophylaxis