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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
Define CP
Non-progressive disorder, but secondary orthopedic deformities are common
26
Ways brain damage occurs while developing
``` During pregnancy (75%) During childbirth (5%) After birth (15%) ```
27
Brain damage during pregnancy
Infections during pregnancy Insufficient perinatal oxygen Prematurity Rh incompatibility
28
Brain damage during childbirth
Asphyxia during labor and delivery
29
Brain damage after birth
Brain injuries during the first two years of life (brain infections, head injuries)
30
Four classifications of cerebral palsy
Spastic Athetoid Ataxic Mixed
31
Spastic CP
Most common type of CP
32
Presentation of spastic CP
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
Athetoid/Dyskinetic CP
Mixed muscle tone (hyper/hypotonia)
34
Presentation athetoid/dyskinetic CP
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
Ataxia CP
Problems with balance, especially while walking
36
Presentation of Ataxia CP
Hypotonia and tremors Motor skills might be difficult Difficulty with visual/auditory processing of objects Instability in balance/relation to gravity
37
Classical symptoms of CP
Spasticity Unsteady gait Dysarthria Decreased muscle mass
38
Most common manifestations of CP
Ataxia | Spasticity
39
CP in newborns & babies
Floppy movements Unable to roll over Unable to sit, crawl, or walk Birth defects
40
CP in older children
Walking with one foot Walking on the toes Muscle tone that is too stiff or floppy
41
Secondary symptoms of CP
``` Seizures Spasms Other involuntary movements Speech or communication disorders Hearing/vision impairments Cognitive disabilities Learning disabilities Behavioral disorders ```
42
Diagnosis of CP
``` 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
Reflexes for infants
``` Moro reflex Walking reflex Rooting reflex Sucking reflex Tonic neck reflex Palmar grasp Babinski ```
44
Imaging findings in CP
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
Prognosis for CP
Brain damage does not progress | Symptoms DO become worse
46
Treatment of CP
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
Define amyotrophic lateral sclerosis (Lou Gehrig's Disease)
Progressive, fatal, neurodegenerative disease caused by degeneration of motor neurons in the CNS that control voluntary muscle movement
48
What does ALS attack?
Attacks nerve cells in the brain and spinal cord
49
What does ALS cause?
Muscle weakness Atrophy Inability to function
50
Is cognitive function spared in ALS?
``` Generally yes Frontotemporal dementia (5%) Subtle cognitive changes (30%) ```
51
Approximate age of diagnosis of ALS
40-70 years | Men > women
52
Who are at greater risk for developing ALS?
Gulf War veterans | Athletes
53
Earliest symptoms of ALS
``` Obvious weakness or muscle atrophy Muscle fasciculation Cramping Stiffness of affected muscles Muscle weakness Slurred/nasal speech ```
54
Bulbar onset of ALS
Dysphagia Slurred, nasal, quieter speech Loss of tongue mobility
55
Neurologic testing for ALS
EEG EMG Nerve conduction velocity MRI
56
Slowing the progression of ALS
Riluzole( Rilutek) | Reduce damage to motor neurons by decreasing the release of glutamate via activation of glutamate transporters
57
What does Wernicke-Korsakoff Syndrome result from?
Chronic alcoholism | Deficiency of thiamine
58
Wernicke-Korsakoff Syndrome is characterized by
Confusion Amnesia Confabulation
59
Other features of Wernicke-Korsakoff Syndrome include
``` Acute weakness Paralysis of EOM's Nystagmus Ataxia Peripheral neuropathy Diplopia ```
60
Diagnosis of Wernicke-Korsakoff Syndrome
``` Symptoms CBC Coags Serum/urine drug test Liver enzymes CT MRI ```
61
Treatment of Wernicke-Korsakoff Syndrome
Supplemental thiamine | THEN glucose

Neurology (10 decks)

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