11/13 HD, rare conditions, neuroplasticity Flashcards

1
Q

what is neuroplasticity? is it good or bad? what drives neuroplasticity?

A

Ability of neurons to change function, chemical profile, or structure. Can be adaptive or maladaptive. Driven by the genetic code, experience, injury.

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2
Q

What are the features of neuroplasticity in Adults?

A

Injury induced reorganization and recovery of function can occur in adults. Ongoing in normal activity and learning.

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3
Q

What is Diaschisis ?

A

A localized injury creating disruption of a pattern of brain activity.

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4
Q

What can be used to help reduce or eliminate a diaschisis caused by injury?

A

behavioral therapy (forced use)

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5
Q

review: what are basic components of the nervous system?

A

10% neurons, 90% glia. Astrocytes.

Oligodendrocytes & Schwann cells. Microglia.

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6
Q

Review: what are basic parts of a neuron and how do they work with neuroplasticity?

A

Soma. Dendrites: Spines as a site for plasticity to occur. Axons: Presynaptic terminal as a site for plasticity to occur.

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7
Q

What is Synaptogenesis?

A

Formation of new synapses, not new blood supply: Axonal sprouting and regeneration. Dendritic sprouting. Dendritic spine alterations. A normal process w/ synaptic pruining.

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8
Q

what happens in neurogenisis?

A

Neural stem cells develop

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9
Q

What is angiogenesis?

A

Blood vessel proliferation. Correlates with amount of neurogenesis. Serves as supporting pathway for new neuron migration.

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10
Q

important concepts in neuro-rehabilitation

A

use behavioral training techniques, activate the excitatory system, limit inhibitory system (learned non-use). introduce the right functional activity at the right time to enhance cortical reorganization.

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11
Q

what are the guidelines for rehabilitation of a paretic hand post CVA?

A

Training of the hand should begin early, include sensory stimulation, move toward complexity of motor task. Early intervention may prevent painful shoulder, spasticity and reduce neglect.

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12
Q

What does FITT stand for in neuro rehab?

A

Frequencty, Intensity, Time, Type.

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13
Q

What are the FITT guidelines for LE rehab?

A

Frequency: 2-5 times per week for 4 weeks. Intensity: highest tolerable speed (80-85% predicted HR max, RPE 17). Time: 45 minutes. Type: Treadmill
(Rule of thumb: gait speed <.2 m/s, 40% BWS may be helpful)

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14
Q

What are FITT guidelines for UE rehab?

A

Frequency: 3 times per week for 6 weeks
Intensity: >/= 300 repetitions per session
Time: 60 minutes
Type: supervised, massed practice of functional daily tasks.
Graded and progressed for each participant
Included reaching, grasping, moving/ manipulating, releasing objects.

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15
Q

What are the benefits of using robotics in neuro rehab?

A

Robotics allow benefits from repetitive motion.
Provide sensorimotor stimulation.
Consistent and reproducible practice.
Objective quantification

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16
Q

What are 8 intervention principles in neuo rehab?

A

Use it or lose it. Use it and improve it. Specificity, Repetition, Intensity, Timing, Salience, and Age all matter.

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17
Q

give an example of a patient for whom neuro rehab principles may not apply?

A

Someone with MS and a blunted response to exercise would not work for this person.

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18
Q

name 4 rare infectious disorders of the nervous system.

A

Meningitis, Encephalitis, Brain Abscess, Prion Disease.

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19
Q

What are 3 categories of neoplasms that, in rare cases, affect the nervous system?

A

Primary tumors
Secondary tumors
Paraneoplastic syndromes

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20
Q

what is meningitis?

A

The meninges of the brain and spinal cord become inflamed. Across the BBB (blood brain barrier so immune system not effective).

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21
Q

what are the cardinal signs of meningitis?

A

Headache, fever, stiff and painful neck. (from Fuller text –>) Often pain in lumbar area and posterior thigh. If infection affects brainstem centers than can see seizures, coma, vomiting, papilledema, cranial nerve palsies, and deafness.

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22
Q

What are some clinical tests for meningitis? (from Fuller text, not on slides)

A

Kernig’s sign: pain with combined hip flexion and knee extension in supine (like a hamstring length test). Brudzinski’s sign: flexion of the neck in supine causes flexion of hips and knees b/c of pain.

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23
Q

What are 5 causes of meningitis?

A

Aseptic (viral or fungal), tuberculosis, Bacteria, Parasitic, non-infectious (cancers, head injury, brain surgery)

24
Q

How is meningitis medically managed?

A

Treat as a medical emergency, especially in a child/infant. Lumbar puncture. Rule out fracture, brain abscess, infarction. Viral cause usually less severe. Bacterial cause treated with antibiotics.

25
Q

Meningitis Prognosis?

A

Mortality 5%-25%. 75% have at least one serious neurologic complication. 30% develop cranial nerve palsies . Hearing loss

26
Q

what is Encephalitis ?

A

Acute inflammatory disease of the brain parenchyma caused by direct viral invasion, primarily gray matter

27
Q

what are 2 main types of Encephalitis?

A

Herpes simplex

West Nile Virus

28
Q

What are general signs and symptoms of Encephalitis?

A

Headache, nausea, vomiting, altered consciousness, agitation. Dependent upon area of brain involved: hemiparesis, ataxia, aphasia, seizures

29
Q

How is Encephalitis medically managed?

A

Differential diagnosis is important
MRI, EEG, lumbar puncture
Limited treatment options, supportive care
Prognosis is highly variable

30
Q

What is a brain Abscess?

A

Infectious disease. 2% of intracranial mass lesions. Described as circumscribed, enlarging, focal infections. Produce symptoms similar to tumors in that they are space occupying lesions. Progress more rapidly than tumors. Compromised immune systems have an increased risk: HIV infection, Steroids, chemotherapy.

31
Q

How is a brain abscess medically managed?

A

Monitor intracranial pressure
Imaging, EEG
Antibiotic treatment and surgery

32
Q

What is counter-intuitive about brain abscess symptoms?

A

May not have increased WBC or fever or neck stiffness

33
Q

What is Prion disease?

A

Prions are abnormal pathogenic agents that induce abnormal folding of specific normal cellular proteins (prion proteins) in the brain
Transmissible. Cause rare forms of encephalopathies. Progressive, neurodegenerative and fatal.

34
Q

what are 2 main types of Prion disease?

A

Creutzfeldt-jakob disease

Mad cow disease (bovine spongiform encephalopathy)

35
Q

what is the difference between secondary tumors and Paraneoplastic syndromes?

A

Secondary tumors on the CNS are metastatic tumors from another site. Paraneoplastic syndromes are the indirect effects on the CNS from tumors elsewhere in the body.

36
Q

What is a glioma, and what types of gliomas are there?

A

Gliomas are primary tumors and constitute 40-50% of brain tumors. There are benign or low-grade gliomas, and malignant gliomas, including Glioblastoma Multiforme (GBM) –which are very fast growing and fatal.

37
Q

what is a Meningioma?

A

Slow growing and usually benign

Most common benign brain neoplasms

38
Q

what is a Pituitary adenoma?

A

Benign tumor of anterior pituitary.

39
Q

what is a Neurinoma, and neuroma?

A

Slow growing, benign tumors originating from Schwann cells. Common on CN VIII – acoustic neuromas originating in internal auditory canal.

40
Q

what are the 2 main types of primary intraspinal tumors?

A

Intradural-Intramedullary: Invade the spinal cord.
May span several cord segments

Intradural-Extramedullary: Derived from supporting elements: meninges, nerve sheath.
Cause spinal cord compression.

41
Q

What is Huntington’s Disease (HD)?

A
Neurodegenerative disease of basal ganglia.
Hyperactivity in basal ganglia circuitry
Inherited as autosomal dominant trait
Marker for HD gene has been localized.
Manifested after age 30
42
Q

What are clinical manifestations of Huntington’s Disease (HD)?

A

Choreoathetoid type extraneous movements. Dysarthria, Dysphagia, Cachexia, Urinary incontinence – UTI, Sleep disorders, Apraxia . Gait takes on ataxic, dancing appearance.

43
Q

How does HD affect cognition?

A

Decreased judgment, Loss of memory, Deterioration of speech and writing, Depression, Hostility, Feelings of incompetence, Decrease in IQ, Changes in social behavior.

44
Q

What is cachexia?

A

emaciation, muscle wasting.

45
Q

How many stages of HD are there? What is the presentation of stage 1?

A

5 stages. Stage 1: Able to perform all ADLs , live at home, work

46
Q

What is the presentation of stage 2 HD?

A

Able to perform ADLs, live at home, work at a lower level, needs assistance for finances

47
Q

What is the presentation of stage 3 HD?

A

Needs min assist for ADLs, cannot do IADLs, unable to work, can live at home with support.

48
Q

What is the presentation of stage 4 HD?

A

Needs mod assist for ADLs, may live in care facility.

49
Q

What is the presentation of stage 5 HD?

A

Needs max assist for ADLs, likely in total care facility

50
Q

What is the main drug category for treatment of HD, and what are some examples?

A

Dopamine antagonists:
Perphanazine (block DA receptors)
Haloperidol (block DA receptors)
Reserpine (depletes DA stores)

51
Q

What are the side effects of Dopamine antagonists?

A

Depression, Drowsiness, Parkinson’s type of syndrome, Dyskinesia.

52
Q

What is the United Huntington’s Disease Rating Scale (UHDRS)?

A
Comprehensive examination that looks at:
Cognitive function, Motor function.
Assess the degree of functional ability:
How chorea interferes with function.
Face, extremities.
53
Q

What is the prognosis of HD?

A

Increasing disability from involuntary movements and decreased mentation. Limited medical intervention/side effects. Death from the disease 15-20 years after onset of symptoms. Large incidence of suicide
6% of deaths, 25% of HD attempt once.

54
Q

What are PT interventions for HD?

A

Maintain optimal quality of life. Maintenance of functional skills. Advice to family on adaptive equipment.Prevent falls and infections. Increase stability in shoulders, trunk, neck, and hips-help maintain function.Gait. Responds to rhythmical auditory stimulation. Use of assistive device. Cognitive issues

55
Q

Family and caregiver Education in HD

A

Safety with transfers. Ongoing modifications to techniques. Equipment needs. Support Groups. Referrals to OT, ST, SW, CM. Positioning to prevent skin breakdown and contractures as disease becomes severe.