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ABIM > Neurology > Flashcards

Neurology Flashcards

1
Q

Parkinson disease characteristics

A

At least 2 of the following: Bradykinesia, rigidity, resting tremor, postural reflex abnormality

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2
Q

Parkinson disease brain involvement

A

degeneration of dopaminergic neurons in the substantia nigra of the midbrain

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3
Q

Parkinson disease general characteristics

A

asymmetric signs and symptoms, diminished sense of small, constipation, acting out dreams; these symptoms may precede motor symptoms by years.
May have frequent falls
If dementia in the first year concern got dementia with lewy bodies

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4
Q

Cutaneous finding in parkinsons disease

A

seborrheic dermatitis

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5
Q

Multiple system atrophy

A

severe orthostatic hypotension and ataxia

MRI shows “necrosis” of the putamen and cerebellar atrophy

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6
Q

Progressive supranuclear palsy

A

Unexplained falls backwards, inability to move eyes vertically, parkinonian features

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7
Q

Dementia with lewy bodies

A

early dementia, parkinsonism, hallucinations

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8
Q

Medication induced parkinsonism

A

antiemetics (prochlorperazine, metoclopramide), antipsychotics (haloperidol), reserpine, lithium, methyldopa
Distinguished from Parkinson disease by symmetry of symptoms and absence of typical nonmotor features

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9
Q

Parkinsons treatment

A

Patients <65 start pramipexole and ropinirole (avoid dyskinesias and wearing off effect)
>65 Levodopa + Carbidopa to prevent peripheral conversion of levodpa to dopamine
Deep brain stimulation if patient has motor benefit from levodopa but medication adverse effects

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10
Q

Essential tremor manifestations

A

slowly progressive or stable over time
bilateral postural or kinetic tremor
improves with alcohol
family history positive in 50%
Rigidity and resting tremor are NOT features
Patients <40 with essential tremor should be screened for Wilson disease with serum ceruloplasmin and 24-hour urine copper measurements

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11
Q

Essential tremor treatment

A

propranolol, primidone, topiramate

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12
Q

Huntington disease characteristics

A

autosomal dominant
most common neurodegenerative cause of generalized chorea
progressive dementia and psychiatric symptoms

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13
Q

Huntington disease treatment

A

tetrabenazine and deutetrabenazine

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14
Q

Drug induced dystonia manifestations

A

tardive dyskinesia with choreiform and dystonic craniofacial movements
can be caused by neuroleptic, antiemetic, serotoninergic medications

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15
Q

Drug induced dystonia treatment

A

stop the offending drug

valbenazine, clonazepam, tetrabenazine, anticholinergic agents, clozapine

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16
Q

Cervical dystonia (torticollis)

A

Cervical muscle contractions resulting in abnormal posture of head and neck

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17
Q

Cervical dystonia (torticollis) treatment

A

Botulinum toxin

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18
Q

Tourette syndrome

A

childhood onset
multiple complex motor tics
presence of vocal tics

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19
Q

tourette syndrome treatment

A

cognitive behavioral therapy, reassurance
First-line agents used to treat Tourette syndrome when the associated tics interfere with education, daily function, or work are clonidine, guanfacine, topiramate, and tetrabenazine.
Second-line treatments include antipsychotic agents (such as haloperidol), but their benefit should be weighed against risk of tardive dyskinesia.

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20
Q

Myoclonus

A

Rapid, shock-like, jerky movements of isolated body parts

underlying metabolic disorder, serotonin syndrome, postanoxic, creutzfield jakob disease, corticobasal degeneration

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21
Q

Multiple sclerosis acute treatment

A

Acute: IV methlypredisolone followed by oral steroids

Treat fever/look for infection before starting steroids (could be pseudorelapse)

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22
Q

Multiple sclerosis chronic treatment

A

interferon beta or glatiramer acetate, teriflunomide could also be effective
Add vitamin D to treatment with interferon beta, reduced accumulation of MRI lesions. Recommended for all MS patients
Interferon agents contraindicated in patients with liver disease or depression

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23
Q

Clinical courses of MS

A

Relapsing-remitting: dysfunction lasting weeks then improving, accumulation of disability
Secondary progressive disease: No more relapses, now progressive disability
Primary progressive disease: progressive disability from time of onset

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24
Q

Droxidopa

A

approved for management of neurogenic orthostatic hypotension in Parkinson disease

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25
Q

Dystonic tremor

A

occurs both at rest and with action and is characterized by associated dystonic posturing and the presence of a null point at which change in the position of the affected limb resolves the tremor.
The null point is the position at which the trajectories of the forces caused by dystonic coactivation of agonist and antagonist muscles neutralize each other, which leads to resolution of the tremor.
the action component of tremor has task specificity (worse with use of scissors but spares the handwriting).

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26
Q

Cerebellar tremor

A

characterized by increasing tremor amplitude as the limb approaches the target (terminal intention tremor) and the presence of associated cerebellar symptoms

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27
Q

Parkinsonian tremor

A

prominent at rest

can reemerge after a brief delay when the arms are held in an outstretched position

28
Q

Rubral tremor

A

caused by focal injury to cerebellar outflow pathways and is characterized by a coarse tremor that is present at rest but most severe during action.
prominent proximal component and interferes with various actions, such as feeding, typing, and writing, in a nonselective way.
MRI of the brain reveal a focal causative lesion

29
Q

Psychosis in parkinsons disease

A

Pimavanserin, a nondopaminergic atypical antipsychotic agent and selective serotonin 5-hydroxytryptamine receptor 2A inverse agonist, is the only FDA-approved medication for Parkinson psychosis.

Quetiapine and clozapine also can be considered in this setting
Other atypical antipsychotic agents (including aripiprazole, risperidone, and olanzapine) and all typical (first-generation) antipsychotic agents should be avoided.

30
Q

Periodic limb movements of sleep

A

characterized by periodic leg kicks, often with a stereotyped triple-flexion phenomenology that repeats periodically during sleep
can occur in otherwise healthy persons or be associated with sleep disorders, such as restless legs syndrome, sleep apnea, narcolepsy, and others
If another sleep disorder is present, treatment targeting the associated disorder also improves the periodic limb movements
If no associated sleep disorder is present treatment is only necessary if limb movements cause sleep fragmentation (brief arousals that occur during a sleep period). In the absence of such issues, no further testing or treatment is recommended.

31
Q

Rapid eye movement (REM) sleep behavior disorder

A

A condition associated with loss of the muscle paralysis normally experienced during the REM dream phase of sleep and typically characterized by dream enactment behavior with complex movements and vocalizations

Clonazepam often is used to treat

32
Q

Restless legs syndrome (RLS)

A

A common movement disorder characterized by discomforting sensations in the legs at rest or when falling asleep, an urge to move the legs, and immediate relief after moving the legs or walking.

Patients should be screened for iron deficiency and receive iron supplements in the presence of deficiency or even low-normal serum ferritin levels.

33
Q

Neuromyelitis optica (Devic disease)

A

Recurrent episodes of myelitis and optic neuritis without the brain lesions typical of MS; NMO-IgG autoantibody may be present

34
Q

Idiopathic transverse myelitis

A

Subacute onset of weakness, sensory changes, and bowel/bladder dysfunction, typically after a viral infection

Distinguished from MS by the presence of complete myelitis, no oligoclonal bands or elevated IgG index in the CSF, and no lesions on brain MRI

35
Q

Vitamin B12 deficiency

A

Paresthesias, lower-extremity weakness, and gait instability
Findings may include paraparesis, vibration and position sense loss, and sensory ataxia.
Anemia may be absent
Check methylmalonic acid and homocysteine levels in patients with borderline B12 levels

36
Q

Copper deficiency

A

Mimics vitamin B12 deficiency

May develop after bariatric surgery or from excessive zinc ingestion

37
Q

Infarction of the spinal cord

A

Acute onset of flaccid paralysis or weakness and pinprick sensation loss below the level of the infarction
Potential causes include emboli, hypotension during cardiovascular/aortic surgery, and AV malformations

38
Q

Amyotrophic Lateral Sclerosis Characteristics

A

The defining characteristic is the combination of upper motor neuron signs (e.g., hyperreflexia, spasticity, and extensor plantar response) coexistent with lower motor neuron findings (e.g., atrophy and fasciculation)

Sensory deficits are characteristically absent

Muscle weakness usually begins distally and asymmetrically, although 20% of patients have bulbar-onset ALS with difficulty speaking and swallowing

Fasciculations in the absence of associated muscle atrophy or weakness are not caused by ALS.
Weakness in the absence of fasciculations is not a result of ALS.

39
Q

Amyotrophic Lateral Sclerosis Treatment

A

Riluzole may increase survival by about 3 months.

Begin noninvasive ventilatory support for patients with respiratory insufficiency.

Placement of a percutaneous endoscopic gastrostomy tube is indicated when weight loss or swallowing difficulty occurs.

40
Q

Myasthenia Gravis Characteristics

A

MG is an autoimmune disease caused by antibodies directed against the acetylcholine receptor, which results in impaired neuromuscular transmission.

Characteristic findings of MG include:

  • ptosis or diplopia (first manifestation in most patients)
  • muscle weakness, including dysphagia and dyspnea
  • positive anti–acetylcholine receptor antibody titer (found in 90% of patients; negative titer does not rule out MG)
  • normal deep tendon reflexes and sensation
  • decremental response to repetitive stimulation on EMG
41
Q

Myasthenic crisis

A

may include rapidly progressive respiratory failure, can occur as part of the natural history of myasthenia or be triggered by infection, surgery, or medications.

Look for aminoglycosides, quinolones, magnesium, β-blockers, or calcium channel blockers as precipitants of myasthenic crisis.

Myasthenic crisis and refractory disease should be treated with plasmapheresis or IV immune globulin.

Pyridostigmine monotherapy should be avoided in those with myasthenic crisis because the drug increases respiratory secretions.

42
Q

Myasthenia Gravis Tests to perform

A

Single-fiber EMG can establish the diagnosis.

Look for elevated serum TSH levels because of the association of MG with autoimmune thyroid disorders.

Perform CT of the chest to detect thymoma.

43
Q

Myasthenia Gravis Treatment

A

Pyridostigmine is the initial therapy.

Thymectomy is indicated if a thymoma is found on imaging.

Myasthenic crisis and refractory disease should be treated with plasmapheresis or IV immune globulin.

Pyridostigmine monotherapy should be avoided in those with myasthenic crisis because the drug increases respiratory secretions.

44
Q

Lambert-Eaton syndrome

A

involves progressive proximal weakness and diminished tendon reflexes that improve with repetitive movement of affected muscles.

Diagnosis is confirmed by detection of serum anti–voltage-gated calcium channel antibodies and the EMG finding of facilitation of motor response to rapid repetitive stimulation.

Most patients with this syndrome have an undetected malignancy, typically SCLC.

45
Q

Myasthenia vs botulism

A

Botulism starts with cranial nerve involvement, including diplopia, dysphagia, and sluggish or nonreactive pupils, whereas the pupils are normal in MG.

46
Q

Multiple sclerosis–related fatigue

A

The most common medications of this type used (off-label) in MS are modafinil, armodafinil, and amantadine. For fatigue that is refractory to these medications, amphetamine stimulants, such as methylphenidate, also can be considered.

47
Q

Tardive dyskinesia

A

can be caused by exposure to dopamine-blocking agents, such as neuroleptic and antiemetic agents, and may persist for more than 6 months after removal of the offending medication or become permanent.

Pharmacologic treatment of tardive dyskinesia is often unsatisfactory, but options include clonazepam, tetrabenazine, valbenazine, anticholinergic agents, and clozapine.

48
Q

Dalfampridine

A

significantly improved timed 25-foot walking speeds in patients with multiple sclerosis and gait impairment

rare adverse effect of seizures and should not be used in patients with kidney impairment, given the reduced clearance of the drug and resultant potentially higher rate of seizures.

49
Q

Pseudobulbar affect

A

Pseudobulbar affect, a less common symptomatic manifestation of MS, can act as a significant impediment to social interaction in patients with MS. This symptom manifests as uncontrolled fits of laughter or crying that occur without distinct or appropriate triggers. A successful trial of the combination agent dextromethorphan-quinidine has led to FDA approval of the use of this pharmacotherapy for pseudobulbar affect in MS. It is not effective for improving or maintaining ambulation.

50
Q

First line treatment for relapsing-remitting MS

A

Generally, self-injection medications (interferon beta or glatiramer acetate) are recommended as first-line agents for relapsing-remitting multiple sclerosis because of their favorable risk profiles.

51
Q

First line treatment for progressive MS

A

Ocrelizumab is the only available therapy for primary progressive multiple sclerosis (MS)

mitoxantrone is the only FDA-approved therapy for secondary progressive MS

52
Q

Natalizumab

A

Natalizumab is a highly effective treatment in multiple sclerosis that causes a two-thirds reduction in relapse rates, slowing of disability progression by approximately 40%, and a reduction in MRI activity of approximately 90% compared with placebo; it is typically limited to use as a second-line agent because of the risk of progressive multifocal leukoencephalopathy.

53
Q

multiple sclerosis–associated spasticity

A

Muscle relaxants, such as baclofen, tizanidine, cyclobenzaprine, and the benzodiazepines, can help treat multiple sclerosis–associated spasticity due to corticospinal tract damage.

54
Q

Peripheral neuropathy

A

may present with pain, paresthesias, weakness, or autonomic dysfunction

Neuropathies can be classified by:

  • distribution of sensorimotor deficits (symmetric vs asymmetric, distal vs proximal, focal vs generalized)
  • pathology (demyelinating vs axonal)
  • size of nerve fibers involved (large vs small fibers)
  • family history
  • autonomic involvement
55
Q

Mononeuropathy

A

isolated disorders affecting a single peripheral nerve

most frequently caused by nerve entrapment or compression (carpal tunnel syndrome)

56
Q

Mononeuropathy multiplex

A

involves multiple noncontiguous peripheral nerves, either simultaneously or sequentially

This is often the result of a systemic disease. Consider vasculitis (especially if painful), lymphoma, amyloidosis, sarcoidosis, Lyme disease, HIV, leprosy, and diabetes”

57
Q

Polyneuropathy

A

refers to a diffuse, generalized, and usually symmetric peripheral neuropathy
Polyneuropathy is often a manifestation of systemic disease (e.g., diabetes, vitamin B12 deficiency) or exposure to a toxin (e.g., alcohol) or medication (e.g., chemotherapy)
EMG and nerve conduction velocity can be helpful to characterize the type (axonal or demyelinating), severity, and distribution of the disease
Other routine tests include vitamin B12 level, SPEP, UPEP, ESR, and blood glucose level

58
Q

Guillain-Barre Syndrome

A

Acute, ascending, areflexic paralysis and paresthesias

Often preceded by GI illness (usually Campylobacter infection)

CSF shows elevated protein and a normal cell count (albuminocytologic dissociation)

Treat with plasma exchange or IVIg

59
Q

Chronic inflammatory demyelinating polyneuropathy

A

Progressive proximal motor and sensory neuropathy that evolves over months

Initial EMG and CSF findings similar to Guillain-Barré syndrome

Treat with prednisone, plasma exchange, or IVIg

60
Q

Paraproteinemic Neuropathy

A

Symmetric distal sensory neuropathy in the setting of MGUS, multiple myeloma, amyloidosis, and cryoglobulinemia

Treat the underlying disorder

61
Q

Peripheral neuropathy treatment

A

Only pregabalin, duloxetine, and tapentadol (extended release) are FDA approved for the treatment of painful neuropathy

62
Q

Small cell lung cancer associated neurologic paraneoplastic syndromes

A

dementia, chorea, ataxia, brainstem encephalitis, and neuropathies, among others.

The antibodies associated with these syndromes include anti-Hu, anti-LGI1 (voltage-gated potassium channel), anti-CRMP5 antibodies and rarely the anti-NMDAR antibody.

63
Q

Immune-mediated necrotizing myopathy

A

a form of statin myopathy that is associated with antibodies to hydroxymethylglutaryl coenzyme A reductase
biopsy evidence of muscle necrosis without inflammation

treatment with a glucocorticoid or other immunosuppressive agents can reverse the myopathy.

64
Q

Idiopathic brachial plexopathy

A

characterized by subacute severe pain followed by resolution of pain and progressive weakness and atrophy involving the shoulder girdle and upper extremity muscles; this syndrome often is triggered by a preceding event, such as an infection or surgery

65
Q

Diabetic mononeuropathy

A

Acute or subacute pain and paresthesia in a dermatomal pattern in the thoracic or abdominal region in a patient with diabetes mellitus and no evidence of herpes zoster is most likely due to diabetic mononeuropathy

66
Q

Miller Fisher variant of Guillain-Barré syndrome

A

typically presents with subacute ataxia, areflexia, and ophthalmoplegia, with or without diffuse weakness

Antibodies to GQ1b (a ganglioside component of nerve) are present in more than 85% of patients. The patient’s findings are not compatible with the Miller Fisher variant.

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