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Neurology > Miscellaneous Neurological Disorders > Flashcards

Miscellaneous Neurological Disorders Flashcards

1
Q

Multiple Sclerosis

A

Most common acquired disease of myelin

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2
Q

How demyelination occurs

A

Body mistakenly directs antibodies and WBCs against proteins in the myelin sheath
Results in inflammation and injury to the sheath

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3
Q

Areas of myelination are found where?

A

White matter of the brain, spinal cord, and optic nerve

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4
Q

Pathogenesis of MS

A

Peri-vascular infiltrates by lymphocytes and monocytes
MHC antigen expression
HLA-DR2

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5
Q

How is MS characterized?

A

Relapses with some degrees of recovery

Progresses to continual disease

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6
Q

Areas commonly affected in MS

A 
Optic nerve
Corticobulbar tracts
Corticospinal tracts
Cerebellar tracts
Spinocerebellar tracts
Longitudinal fasciculus
Posterior cell columns of the spinal cord
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7
Q

Who is most commonly affected?

A

Ages 15-50

More common in women

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8
Q

Geographical factors where MS is commonly found

A 
Temperate climates
Europe
Southern Canada
Norther US
Southeastern Australia
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9
Q

Environmental factors in MS

A

Viruses

Bacteria

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10
Q

Symptoms of MS

A 
Weakness, numbness, tingling, or unsteadiness in a limb
Unilateral visual impairment
Fatigue
Spastic paraparesis
Diplopia
Disequilibrium
Muscle weakness
Sphincter disturbances
Dysarthria
Mental disturbance
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11
Q

Signs of MS

A 
Optic neuritis
Opthalmoplegia
Nystagmus
Spasticity or hyperreflexia
Babinski sign
Absent abdominal reflexes
Labile/changed mood
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12
Q

Onset of MS

A

Younger patients- subacute or acute

Older patients- insidiously progressive myelopathy

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13
Q

Forms of the disease

A

Secondary progressive disease- acute relapses

Primary progressive disease- steady progression from onset

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14
Q

CSF results

A 
Usually normal but can have
Protein elevations
Lymphocytosis
Elevated IgG
Myelin antibodies
Oligoclonal bands
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15
Q

MS diagnosis requirements

A

Intermittent or progressive CNS symptoms supported by evidence of two or more CNS white matter lesions occurring in an appropriately aged patient

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16
Q

Treatment categories of MS

A

Treat acute symptoms
Modify course of disease
Interrupt progressive disease
Treat continuing symptoms

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17
Q

Minimal affected patients and treatment

A

No specific treatment
Encourage to maintain healthy lifestyle
Physical therapy

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18
Q

Treatment of acute symptoms

A

Corticosteroids

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19
Q

Treatment of modifying disease

A

Interferon 1a
Interferon 1b
Glatiramer acetate

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20
Q

Treatment of progressive disease

A 
Immunosuppressants such as:
Methotrexate (Rheumatrex)
Cyclophosphomide (Cytoxan)
Mitoxantrone (Novantrone)
Azathioprine (Imuran)
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21
Q

Tysabri (Natalzumab) in MS

A

Lab produced monoclonal antibody

Hamper movement of potentially damaging immune cells from the bloodstream across the “blood-brain-barrier”

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22
Q

Symptom treatment of MS

A 
Dantrolene (Muscle relaxant)
Baclofen (muscle relaxant)
Modofinil (provigil)- CNS stimulant
Amantadine (anti-viral)
(Bethanechol)
Antidepressants
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23
Q

Cerebral Palsy cause

A

Caused by abnormalities in parts of the brain that control muscle movements

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24
Q

CP

A

Disease of childhood

Most children born with it but not detected

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25
Q

Define CP

A

Non-progressive disorder, but secondary orthopedic deformities are common

26
Q

Ways brain damage occurs while developing

A 
During pregnancy (75%)
During childbirth (5%)
After birth (15%)
27
Q

Brain damage during pregnancy

A

Infections during pregnancy
Insufficient perinatal oxygen
Prematurity
Rh incompatibility

28
Q

Brain damage during childbirth

A

Asphyxia during labor and delivery

29
Q

Brain damage after birth

A

Brain injuries during the first two years of life (brain infections, head injuries)

30
Q

Four classifications of cerebral palsy

A

Spastic
Athetoid
Ataxic
Mixed

31
Q

Spastic CP

A

Most common type of CP

32
Q

Presentation of spastic CP

A

Damage to corticospinal tract, motor cortex or pyramidal tract
Affect nervous system ability to receive gamma amino butyric acid
Hypertonic
Spastic hemiplegias
Spastic diplegia (LE)
Spastic quadriplegia

33
Q

Athetoid/Dyskinetic CP

A

Mixed muscle tone (hyper/hypotonia)

34
Q

Presentation athetoid/dyskinetic CP

A

Have trouble holding themselves in upright, steady position for sitting/walking
Show involuntary motions
Lots of work & concentration to get hand to a certain spot
May not be able to hold onto things

35
Q

Ataxia CP

A

Problems with balance, especially while walking

36
Q

Presentation of Ataxia CP

A

Hypotonia and tremors
Motor skills might be difficult
Difficulty with visual/auditory processing of objects
Instability in balance/relation to gravity

37
Q

Classical symptoms of CP

A

Spasticity
Unsteady gait
Dysarthria
Decreased muscle mass

38
Q

Most common manifestations of CP

A

Ataxia

Spasticity

39
Q

CP in newborns & babies

A

Floppy movements
Unable to roll over
Unable to sit, crawl, or walk
Birth defects

40
Q

CP in older children

A

Walking with one foot
Walking on the toes
Muscle tone that is too stiff or floppy

41
Q

Secondary symptoms of CP

A 
Seizures
Spasms
Other involuntary movements
Speech or communication disorders
Hearing/vision impairments
Cognitive disabilities
Learning disabilities
Behavioral disorders
42
Q

Diagnosis of CP

A 
Several months to years
Parents/caregivers first to notice
Floppy or stiff muscle tone
Reflexes
Preference for hand
Careful medical hx
CT/MRI/ultrasound
43
Q

Reflexes for infants

A 
Moro reflex
Walking reflex
Rooting reflex
Sucking reflex
Tonic neck reflex
Palmar grasp
Babinski
44
Q

Imaging findings in CP

A

Thin shafts of bones
Metaphyses enlarged
Articular cartilage may atrophy
Exhibit variety of angular joint deformities
Spasticity and abnormal gait hinder proper bone & skeletal development
Shorter in height
Bones grow at differing lengths

45
Q

Prognosis for CP

A

Brain damage does not progress

Symptoms DO become worse

46
Q

Treatment of CP

A

PT, OT, ST
Drugs to control seizures, relax muscle spasms, alleviate pain
Surgery to correct anatomical abnormalities
Braces/orthotic devices
Wheelchairs/rolling walkers
Communication aids

47
Q

Define amyotrophic lateral sclerosis (Lou Gehrig’s Disease)

A

Progressive, fatal, neurodegenerative disease caused by degeneration of motor neurons in the CNS that control voluntary muscle movement

48
Q

What does ALS attack?

A

Attacks nerve cells in the brain and spinal cord

49
Q

What does ALS cause?

A

Muscle weakness
Atrophy
Inability to function

50
Q

Is cognitive function spared in ALS?

A 
Generally yes
Frontotemporal dementia (5%)
Subtle cognitive changes (30%)
51
Q

Approximate age of diagnosis of ALS

A

40-70 years

Men > women

52
Q

Who are at greater risk for developing ALS?

A

Gulf War veterans

Athletes

53
Q

Earliest symptoms of ALS

A 
Obvious weakness or muscle atrophy
Muscle fasciculation
Cramping
Stiffness of affected muscles
Muscle weakness
Slurred/nasal speech
54
Q

Bulbar onset of ALS

A

Dysphagia
Slurred, nasal, quieter speech
Loss of tongue mobility

55
Q

Neurologic testing for ALS

A

EEG
EMG
Nerve conduction velocity
MRI

56
Q

Slowing the progression of ALS

A

Riluzole( Rilutek)

Reduce damage to motor neurons by decreasing the release of glutamate via activation of glutamate transporters

57
Q

What does Wernicke-Korsakoff Syndrome result from?

A

Chronic alcoholism

Deficiency of thiamine

58
Q

Wernicke-Korsakoff Syndrome is characterized by

A

Confusion
Amnesia
Confabulation

59
Q

Other features of Wernicke-Korsakoff Syndrome include

A 
Acute weakness
Paralysis of EOM's
Nystagmus
Ataxia
Peripheral neuropathy
Diplopia
60
Q

Diagnosis of Wernicke-Korsakoff Syndrome

A 
Symptoms
CBC
Coags
Serum/urine drug test
Liver enzymes
CT
MRI
61
Q

Treatment of Wernicke-Korsakoff Syndrome

A

Supplemental thiamine

THEN glucose

Neurology (10 decks)

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