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711 Adult Neurological Rehab > Progressive Disorders of the CNS > Flashcards

Progressive Disorders of the CNS Flashcards

1
Q

3 nuclei that make up dorsal or sensorimotor basal ganglia

A
  • caudate nucleus
  • putamen
  • globus pallidus
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2
Q

BGD Symptoms

A
  • problems with controlling speech, movement, and posture
  • difficulty starting, stopping, or sustaining movement
  • increased muscle tone and rigidity
  • memory loss and trouble finding words
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3
Q

Basal Ganglia Disease (BGD) results in difficulty in

A
  • initiating, continuing, or stopping movement.
  • muscle tone (rigidity)
  • increased involuntary movements (tremor, chorea)
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4
Q

Motor disorders of BG result in disequilibrium between ___ and ____ movement.

A

inhibitory and excitatory

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5
Q

Cerebellar dysfunctions: Lesions affect which areas?

A

Lesions are varied and may affect the Neocerebellar (Posterior lobe), Paleocerebellar (anterior lobe), and Archicerebellar (Flocculonodular lobe).

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6
Q

Cerebellar dysfunctions: Signs & symptoms of neocerebellar lesions (posterior lobe)

A

Ipsilateral ataxia, Ipsilateral hypotonia & hyporeflexia, Dysmetria, Adiadochkinesia, movement decomposition, asthenia, intention tremors, rebound phenomenon, ataxic gait, staccato voice

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7
Q

Cerebellar dysfunctions: Signs & symptoms of paleocerebellar lesions (anterior lobe)

A

Disturbances in extensor tone (b/c this lobe receives the Spinocerebellar tracts – which when lost result in an ↑ in extensor tone.)

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8
Q

Cerebellar dysfunctions: Signs & symptoms of archicerebellar lesions (flocculonodular lobe)

A

Uncoordinated trunk movements – ataxia. Balance deficits d/t loss of vestibular input from vestibular nuclei, cuneocerebellar tract, and rostral cerebellar tract

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9
Q

PT/OT management of cerebellar dysfunctions

A

Added weight to help decrease tremor (but performance declines due to the added weight); Strengthening (help with deconditioning, weakness, or spasticity)

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10
Q

ALS Basic Info

A
  • destruction of UMN and LMN (degeneration of anterior horn cells and descending corticobulbar and corticospinal)
  • usually occurs after 50 yrs but can be younger
  • Causes weakness and atrophy to the body
  • spasticity, hyperreflexia
  • affects distal (limbs) to proximal (whole body)
  • loss of voluntary control
  • one of 1st signs is thenar eminence wasting
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11
Q

Etiology of ALS

A
  • unknown (viral/autoimmune/toxic)

- 5-10% genetic (autosomal dominant)

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12
Q

Stage I of ALS

A

early disease, mild focal weakness, asymmetrical distribution, symptoms of hand cramping and fasiculations

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13
Q

Stage II of ALS

A

moderate weakness in groups of muscles, some wasting (atrophy) of muscles; modified independence with assistive devices

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14
Q

Stage III of ALS

A

severe weakness of specific muscles, increasing fatigue, mild to moderate functional limitations, ambulatory

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15
Q

Stage IV of ALS

A

severe weakness and wasting of LEs, mild weakness of UEs; moderate assistive and assistive devices, wheelchair user

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16
Q

Stage V of ALS

A

progressive weakness with deterioration of mobility and endurance, increased fatigue, moderate to severe weakness of whole limbs and trunk, spasticity, hyperreflexia, loss of head control, maximal assist

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17
Q

Stage VI of ALS

A

bedridden, dependent ADLs, FMS; progressive respiratory distress, mimics Locked-In Syndrome

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18
Q

Examination of ALS

A
  • pt must have s/s of both UMN and LMN destruction
  • determine stage patient is in using ALS Functional Rating Scale
  • MMT
  • ROM
  • Reflexes
  • Purdue Pegboard Test
  • Pulmonary function
  • Speech evaluation
  • Ashworth Spasticity scale
  • CN’s; especially VII, IX, X, XI, XII
  • Gait: timed test
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19
Q

ALS Functional Rating Scale (ALSFRS)

A
  • assess disease progression and function across 10 functional categories
  • Scored 0 (loss of function) to 4 (normal function)
  • 40 maximal score
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20
Q

Motor Learning Stage 1 of ALS

A
  • independent of mobility and ADLs
  • Active ROM
  • Cont. normal activities
  • stretching of affected joints
  • resistive exercises to unaffected mm
  • aerobic activities
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21
Q

Motor Learning Stage 2 of ALS

A
  • moderate weakness in groups of mm
  • assess for use of assistive devices
  • continue stage 1 activities
  • increased need for caregiver assistance
  • exercise 2-3 times per day with rest in between
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22
Q

Motor Learning Stage 3 of ALS

A
  • continued ambulation but severe weakness in mm groups
  • foot drop or hand weakness
  • goals is to keep pt physically independent
  • use of splints, orthotics
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23
Q

Motor Learning Stage 4 of ALS

A
  • severe weakness of legs, involvement of arms
  • WC
  • Cont. AROM and PROM to prevent contractures
  • strengthening
  • integumentary
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24
Q

Motor Learning Stage 5 of ALS

A
  • progressive weakness of mobility and endurance
  • inability to transfer
  • pain due to cramping and contracture
  • stretching, splinting, STM, orthotic
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25
Q

Motor Learning Stage 6 of ALS

A
  • bed ridden, max assist, hospital bed, frequent repositioning, pain management, postural drainage, coughing techniques, airway clearance
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26
Q

PT Goals for ALS

A
  • maintain respiratory function
  • provide for nutritional needs
  • prevent indirect impairments
  • provide moderate exercise program
  • teach energy conservation
  • maintain maximal functional independence
  • symptomatic treatment
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27
Q

ALS: Respiratory Function

A
  • may require air way clearance techniques
  • cough facilitation
  • breathing exercises
  • chest stretching
  • suctioning
  • incentive spirometry
  • long term mechanical ventilation
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28
Q

ALS Exercise Precautions

A
  • monitor fatigue levels closely
  • avoid overwork injury
  • limited positions with decreased pulmonary functioning
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29
Q

AIDS: Motor learning and recovery of function

A
  • motor learning is slower in pt’s with HIV
  • may have lack of coordination so would want to have adaptive or compensatory mechanisms for them to complete activities
  • physical activity is good
  • KEEP THEM ACTIVE
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30
Q

Alcoholic Ataxia: Pathogenesis and History

A
  • a loss of coordination in performing voluntary movements associated with peripheral neuritis as a result of alcoholism
  • similar form of ataxia may occur with neuritis resulting from other toxic agents
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31
Q

S/S of Alcoholic Ataxia

A
  • wide-footed, unsteady gait
  • slurred speech
  • clumsiness of their hands
  • double vision
  • legs often affected pt states “slow legs”
  • peripheral neuropathy (especially in feet and legs)
  • loss in vibration sense and DTR
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32
Q

Basal Ganglia Disease

A
  • common disorders: Parkinson’s, Huntington Chorea, and dystonias
  • affect 1 million people in US
  • Impairments in: muscle tone, movement coordination and motor control, postural stability, presence of extraneous movement
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33
Q

What is Parkinson’s Disease (PD)?

A

Chronic progressive disease of CNS with degeneration of dopaminergic substantia nigra neurons and nigrostriatal pathways

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34
Q

With degeneration of substantia nigra, there is a ___ of dopamine within the BG corpus striatum - With PD

A

Deficiency

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35
Q

Loss of inhibitory dopamine results in ____ excitatory output from cholinergic system - with PD

A

excessive

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36
Q

Characteristics of PD

A

rigidity (leadpipe or cogwheel)
bradykinesia
restring tremor
impaired postural reflexes

its slowly progressive

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37
Q

Tool(s) assessing dynamic balance

A

Tandem Walking and Four Square Step Test

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38
Q

Cognitive/Behavioral status in pts. with PD

A
  • intellectual impairments/dementia in advance stages
  • memory
  • bradyphrenia (slowing of thought processes)
  • depression
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39
Q

Communication with PD

A
  • Dysarthria
  • Hypophonia (decreased volume)
  • Mutism in advanced stages
  • Mask like face with infrequent blinking and expression
  • Writing becomes progressively smaller
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40
Q

Oromotor Control with PD

A
  • Dysphagia

- Problems in chewing and swallowing

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41
Q

ROM, Deformity associated with disuse and inactivity with PD

A
  • Contractures common in flexors, adductors
  • Persistent posturing in kyphosis with forward head
  • Many patients osteoporotic with high risk of fracture
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42
Q

Sensation/Perceptual Function with PD

A
  • Aching and stiffness
  • Abnormal sensations (cramp like sensations)
  • Problems in spatial organization
  • Perception of vertical
  • Extreme restlessness (akathisia)
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43
Q

Vision with PD

A
  • Blurring
  • Cogwheeling eye pursuit
  • Eye irritation from decreased blinking
  • Decreased pupillary reflexes
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44
Q

Lead Pipe rigidity

A
  • smooth resistance to passive movement that is independent of velocity
  • can be made more obvious with voluntary movement or mental task
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45
Q

Cogwheel rigidity

A

ratcheting through ROM due to subtle tremor superimposed on the rigidity

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46
Q

Gait with PD

A
  • Characterized by poverty of movement
  • Generalized lack of extension
  • Festination is common
    • -Abnormal, involuntary increase in the speed of walking, often with forward acceleration, but may occur with backward progression)
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47
Q

Name clinical features of cerebellar dysfunctions.

A

hypotonia; asthenia; ataxia; truncal ataxia; dysmetria; gait disturbance; movement decomposition; dysdiadochokinesia; slowed speech enunciation w/ a tendency to hesitate at the beginning of a word or syllable; involuntary, rapid oscillation of the eyeballs in a horizontal, vertical, or rotary direction, with the fast component maximal toward the side of the cerebellar lesion

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48
Q

Asthenia

A

muscles tend to be weaker and get tired than most muscles

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49
Q

Ataxia

A

disturbances in gait and decomposition of movement, wide-based gait

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50
Q

Truncal ataxia

A

Oscillations while sitting or standing; falling may occur toward the side of a unilateral lesion

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51
Q

Dysmetria (definition and way to test for it)

A

Errors in judging distance with body movements, tested by finger-to-nose test, which may result in underestimation (hypometria) or overestimation with transient overshoot (hypermetria)

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52
Q

Describe myasthenia gravis and its etiology.

A

A neuromuscular junction disorder characterized by progressive muscular weakness and fatigability on exertion. Etiology: autoimmune antibody-mediated attack on acetylcholine receptors at neuromuscular junction.

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53
Q

Characteristics of myasthenia gravis

A

Muscular strength worse with continuing contraction, improved with rest.

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54
Q

Describe Generalized myasthenia and its course of progression

A

Usually involves bulbar (extraocular, facial and muscles of mastication) and proximal limb girdle muscles; Course varies: may progress from mild to severe, typically within 18 months

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55
Q

What should be examined in regards to myasthenia gravis?

A

cranial nerves, respiratory function, muscle strength, functional mobility skills, EMG & repetitive nerve stimulation studies

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56
Q

Muscle strength testing for myasthenia gravis

A

Muscle strength: proximal more involved than distal, fatigability, repeated muscle use results in rapid weakness

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57
Q

In regards to myasthenia gravis, EMG and repetitive nerve stimulation studies reveal what?

A

Show abnormal responses to repetitive nerve stimulation (failure of transmission, decreased EMG-recorded responses)

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58
Q

Medical Interventions for myasthenia gravis

A

Acetylcholinesterase inhibitors: pyridostigmine; Corticosteriods: prednisone, methylprednisolone; Immunosuppressents: azathioprine, IV immunoglobulin ( IVIG); Alternative treatments: plasmapheresis ( removal of blood with filtering and separation of cellular elements from plasma; thymectomy.

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59
Q

S and S of Brain Tumor

A

Headaches (usually worse in the morning); Nausea and vomiting; Changes in speech, vision, or hearing; Problems balancing or walking; Changes in mood, personality, or ability to concentrate; Problems with memory; Muscle jerking or twitching (seizures or convulsions); Numbness or tingling in the arms or legs

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60
Q

Describe Tumor Grade I

A

The tissue is benign. The cells look nearly like normal brain cells, and they grow slowly.

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61
Q

Describe Tumor Grade II

A

The tissue is malignant. The cells look less like normal cells than do the cells in a Grade I tumor.

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62
Q

Describe Tumor Grade III

A

The malignant tissue has cells that look very different from normal cells. The abnormal cells are actively growing.

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63
Q

Describe Tumor Grade IV

A

The malignant tissue has cells that look most abnormal and tend to grow quickly.

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64
Q

Astrocytoma

A

The tumor arises from star-shaped glial cells called astrocytes. It can be any grade. In adults, an astrocytoma most often arises in the cerebrum.

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65
Q

Meningioma

A

The tumor arises in the meninges. It can be grade I, II, or III. It’s usually benign (grade I) and grows slowly.

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66
Q

Oligodendroglia

A

The tumor arises from cells that make the fatty substance that covers and protects nerves. It usually occurs in the cerebrum. It’s most common in middle-aged adults. It can be grade II or III.

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67
Q

Medical and Surgical Management for Brain Tumors

A

General Surgery, Radiation, Radiosurgery, Chemotherapy

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68
Q

causes of encephalitis

A

herpes; viruses spread by mosquitoes and ticks.

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69
Q

features of encephalitis (What is resembles, how long it lasts, S&S, etc.)

A

Resembles the flu; Lasts for 2-3 wks; S&S: fever, fatigue, sore throat, stiff neck and back, vomiting, headache, confusion, irritability, unsteady gait, drowsiness, visual sensitivity. More severe symptoms: seizures, muscle weakness, paralysis, memory loss, sudden impaired judgment, and poor responsiveness. Vary from mild to life threatening to mild infection to recover fully. Severe cases will recover but may have damage to their NS.

70
Q

General Aspects of Patient Management for encephalitis

A

Bed mobility, strength, ROM, positioning, transfers; Motor Learning & Recovery of function (varies on factors like age, severity, strength of immune system).

71
Q

Meningitis S&S and other hallmark signs

A

S&S: Vomiting or nausea, confusion or difficulty concentrating, seizures, sleepiness or difficulty waking up, sensitivity to light, lack of interest in drinking and eating, and skin rash in some cases.
Hallmark signs: headache, fever and a stiff neck.

72
Q

Post effects of meningitis

A

Memory loss / difficulty retaining information / lack of concentration, clumsiness / coordination problems, residual headaches, deafness / hearing problems / tinnitus / dizziness, loss of balance, learning difficulties (ranging from temporary learning deficiencies to long term mental impairment), epilepsy / seizures, weakness, paralysis or spasms of part of body, speech problems, Loss of sight/changes in sight.

73
Q

What does levodopa do?

A

Helps decrease the effects of Parkinson’s Disease (by increasing dopamine concentrations)

  • a low protein diet prolongs effects
  • Sinemet is a brand name of Carbidopa-levodopa
74
Q

What are things to be aware of with patients on levodopa?

A
  • DETERIORATION when at end of dose
  • FLUCTUATIONS in symptoms due to dosing
  • On-Off phenomenon
  • Dyskinesia (levodopa-induced after 2-3 years)
75
Q

Side effects of Sinemet (Carbidopa-levodopa)

A
  • Nausea & Vomiting
  • Orthostatic Hypertension
  • Arrhythmias
  • Involuntary Movements
  • Psychoses/Abnormal Behaviors (Hallucinations)
76
Q

What is the On/Off Phenomenon?

A

Sudden changes from normal function to immobility to severe dyskinetic movements that may occur in patients such as those with Parkinson’s Disease.

77
Q

Medical Management of PD

A
  • Dopamine Agonists (bromocriptine, pergolide, mesylate)
  • Anticholinergic drugs (for tremors)
  • Amantadine (+Dopamine Release)
  • Selegiline - Slows disease progression early on
  • DBS - thalamus or subthalamic nucleus
78
Q

PT Interventions for PD?

A

Maintain as normal function as possible!

Examples:

  • Improve strength (PNF, etc.)
  • Minimize secondary impairments
  • Teach compensatory strategies to initiate movement
  • Maintenance program
  • Relaxation skills
  • Improve posture, balance
  • Improve endurance
  • LSVT Big
  • etc.
79
Q

What is MS?

A

Multiple Sclerosis: chronic demyelinating of the CNS

  • Mostly Young Adults (20-40 y/o)
  • Most likely viral and autoimmune
  • These demyelinating lesions (plaques) cause nerve fibers to fatigue rapidly
80
Q

What are the categories of MS?

A

RRMS - Relapsing-Remitting MS: Relapse with full or lots of recovery. Periods between relapses lack disease progression

PPMS - Primary Progressive MS: Disease progresses from onset with hardly or no plateaus/remissions and temporary or no improvements

SPMS - Secondary Progressive MS: Initially relapsing-remitting course, followed by progression at variable rate that may have occasional relapses & remissions

PRMS - Progressive Relapsing MS: Most common in individuals who develop the disease after 40+ y/o. Progressive from onset without clear, acute relapses that may or may not have some recovery or remission

81
Q

What are signs and symptoms of MS?

A

Sensory symptoms: hypoesthesia, paresthesias
Pain: dysesthesias, optic or trigeminal neuritis, chronis pain
Visual Symptoms: blurred or double vision, diminished acuity/ loss of vision, scotoma, nystagmus
Cognitive Symptoms: memory or recall problems, decreased attention and concentration, diminished abstract reasoning, problem solving, judgement, diminished visual-spatial abilities
Emotional Symptoms: depression, pseudobulbar affect, anxiety
Motor Symptoms: weakness or paralysis, fatigue, spasticity, incoordination, intention tremor, impaired balance, gait disturbances
Bladder Symptoms: urinary urgency, nocturia, incontinence
Sexual Symptoms: impotence, decreased libido, decreased vaginal lubrication, impaired ability to achieve orgasm
Bowel Symptoms: constipation, diarrhea, incontinence
Speech and Swallowing: dysarthia, diminished verbal fluency, dysphonia, dysphagia

82
Q

Standardized Tests for MS

A

Expanded Disability Status Scale (EDSS)
Minimum Record of Disability (MRD)
Modified Fatigue Impact Scale

83
Q

Medicine for MS

A

Adrenocorticotropic Hormone (ACTH) + steroids: immunisuppresant to treat flare ups
Interferon Drugs (Avonex, Betaseron, Copaxone): Slow progression and decrease symptoms
Spasticity Management: Baclofen, diazepam (valium), dantrolene, phenol block surgery
Urinary Problems: anticholinergics

84
Q

PT Goals and Interventions for MS

A

Improve/stabilize patient status after relapse, minimize impairments due to disuse and disease progression, examine for UTI and respiratory infection, maintain ROM, prevent contracture, maintain skin integrity, improve respiratory function, education!! (about medicine, AD, techniques, resources), etc.

85
Q

What are some of the factors that allow you to predict a prognosis for MS?

A
  • only 1 symptom = favorable outcome
  • Benign & RRMS most favorable
  • PPMS = unfavorable outcome
  • Younger = more favorable; 40+ = likely to be PPMS
  • Findings at 5 years at most important factors. Pyramidal & Cerebellar signs with multiple site involvement = very poor prognosis
  • MRI: Low total lesion burden, low active lesion formation, negligible myelin/axon less = favorable
86
Q

Huntington’s Disease

A

Fatal autosomal dominant hereditary disorder, insidious onset, occurs in mid 30s-40s.

87
Q

What are the stages of Huntington’s Disease?

A

Stage 1-3: Mild to Moderate
- Increased concerns about cognitive issues, irritiability, chorea

Stage 4-5: Severe

  • Lack of cognitive concerns; late stage dementia
  • Fatal stage (usually due to respiratory issues)
88
Q

PT Goals and Interventions for Huntington’s Disease

A

Strength, flexibility, balance, and coordination
Reduce risk of falls
Increase endurance levels
Posture for respiratory care and for ambulation
Chest physical therapy for respiratory problems
Relaxation techniques
Bobath techniques
Vestibular exercises for balance
Use of supports to improve posture and movement problems
In later stages work on hand muscles to maintain some form of Independence
Creative movement therapy: to help with perceptual problems
Assistive devices
Walker (patient education)

89
Q

BGD Symptoms

A
  • problems with controlling speech, movement, and posture
  • difficulty starting, stopping, or sustaining movement
  • increased muscle tone and rigidity
  • memory loss and trouble finding words
90
Q

Occupational therapy for Huntington’s Disease

A

Training ADLs, eating, and drinking

91
Q

Psychotherapist treatment for Huntington’s Disease

A

Treating behavioral problems & changes in personality

92
Q

T/F? Huntington’s Disease can be stopped.

A

False – There is no cure. Functional recovery is not an option but maintaining the quality of life is important through strengthening, flexibility, and balance/coordination exercises; also adaptive tools for their environment—done through Physical Therapy.

93
Q

Huntington’s Disease: Family Education

A

Appropriate care for this disease; Home environment; Long term care will be needed; Equipment for ambulation will be needed; Good support system; Genetic counseling is advised; Support Groups are available; Will eventually need 24 hour care

94
Q

Suicide is common among patients with what disease?

A

Huntington’s disease

95
Q

Speech Language Therapy interventions for cerebellar dysfunctions

A

Swallowing exercises, dietary modification; Feeding by percutaneous endoscopic gastrostomy (PEG) tube (In advanced cases: feeding via PEG tube can reduce risk of aspiration).

96
Q

Pharmacotherapy for cerebellar dysfunctions

A

Primidone, Beta blockers (proprandolol), benzodiazepines; Other: Appropriate medications may be given for associated symptoms such as spasticity, parkinsonism, dystonia, bladder dysfunction, and orthostatic hypotension.

97
Q

Surgical treatment for cerebellar dysfunctions

A

High-frequency electrical stimulation of the ventral intermediate nucleus of the thalamus, or surgical lesions, can reduce cerebellar tremor. There is no effect on ataxia.

98
Q

Gene/Stem Cell Therapy

A

Not yet used for cerebellar dysfunctions but recent advances have enhanced our understanding of the genetic basis of many of the inherited ataxias, and the possibility of gene therapy is being studied in other neurodegenerative diseases.

99
Q

BGD Motor learning and recovery of function

pharmacology agents help control _____ but not ____

A

general function but not precise motor function

100
Q

BGD Motor learning and recovery of function

A

use self generated movements that require feed forward control

101
Q

Medical Management of ALS

A
  • no effective treatment for disease
  • Riluzole, a glutamate antagonist may slow progression
  • symptomatic relief: spasticity, pain, respiratory failure, mobility, family education
102
Q

ALS Nutritional Needs

A
  • assist in management of dyshpagia

- may require NG tube of percutaneous gastrostomy in later stages

103
Q

Acquired Immunodeficiency Syndrome (AIDS) Signs and Symptoms

A
  • HA
  • diarrhea
  • nausea
  • vomiting
  • fatigue
  • aching muscles
  • sore throat
  • red rash that doesn’t itch
  • flu like symptoms last 2-4 wks
  • confusion, forgetfulness, behavioral changes
  • loss of sensation in extremities
  • atrophy
104
Q

Basic AIDS information

A
  • HIV often leads to AIDS: CD4 drops below 200
  • progressive disease
  • HIV associate with lipodystrophy
  • meds can cause weakness or changes in sensation (HAART)
105
Q

AIDS Exam

A
  • look for rashes on the torso
  • MMT
  • Reflexes
  • Sensory testing
  • CD4 count, viral load, drug resistance
106
Q

AIDS: Pt management

A
  • depends on which stage of the disease the pt is in
  • keep pt emotionally involved in the treatment
  • strengthening program to treat generalized mm weakness
107
Q

AIDS: Education of family

A
  • skin checks, bed mobility, transfers, sterility, keep person active
  • special housing, mental health care, home health care, support groups, med management programs
  • educate pt on how to not spread the disease
108
Q

Examination for Alcoholic Ataxia

A
  • Romberg sign
  • finger to nose test
  • gait assessment (tandem gait)
  • sensory testing
  • DTR
  • MMT to rule out weakness
109
Q

General pt Management for Alcoholic Ataxia

A
  • educate pt to stop drinking
  • improve balance and postural reactions against external stimuli
  • increase postural stabilization following joint stabilization
  • developing UE function
  • develop independent functional gait
  • improve life quality of pt with independent ADLs
110
Q

Hoehn and Yahr classification of stages for PD - Stage I

A

minimal or absent disability, unilateral symptoms

111
Q

Hoehn and Yahr classification of stages for PD - Stage II

A

Minimal bilateral or midline involvements, no balance involvement

112
Q

Hoehn and Yahr classification of stages for PD - Stage III

A

Impaired balance, some restrictions in activity

113
Q

Hoehn and Yahr classification of stages for PD - Stage IV

A

all symptoms present and severe; stands and walks only with assistance

114
Q

Respiratory Status with PD

A
  • Breathing patterns
  • Vital capacity
  • Decreased chest expansion
115
Q

Skin Integrity and Condition, Circulatory Changes with PD

A
  • Edema may occur in lower extremities
  • Increased sweating ( ANS dysfunction)
  • Decubitus ulcers in late stages
116
Q

Balance with PD

A
  • Impaired postural reactions are common (worse with severe rigidity of trunk, lack of trunk rotation)
  • Examine for ability to maintain static and dynamic balance, reactive adjustments and anticipatory adjustments
117
Q

Functional Status with PD

A
  • Overall level of endurance
    • -Fatigue and inability to sustain performance is common
    • -Affected by stress, high effort
    • -cardiovascular deconditioning occurs with long standing disease
118
Q

Tool(s) assessing static balance

A

External Perturbation Test - Push and Release test, Static and Dynamic Posturography, & Single Leg Stance Test

119
Q

Tool(s) assessing static balance in different sensory conditions

A

External Perturbation Test - Pull test

120
Q

Tool(s) assessing dynamic balance in different sensory conditions

A

Clinical Sensory Integration Test

121
Q

Tool(s) assessing static and dynamic balance

A

Sensory Integration Test of Computarised Dynamic Posturography

122
Q

Tool(s) assessing functional static and dynamic balance

A

Functional Reach Test & Berg Balance Scale

123
Q

Tool(s) assessing functional dynamic balance and gait

A

Five Times Sit to Stand Test

124
Q

Tool(s) assessing gait and functional dynamic balance

A

Timed Up and Go Test

125
Q

Tool(s) assessing dynamic balance and gait

A

Dynamic Gait Index

126
Q

What are the purposes of the International Cooperative Ataxia Rating Scale and Brief Ataxia Rating Scale ?

A

Evaluating truncal and extremity ataxia, gait ataxia, nystagmus and talking

127
Q

What are the purposes of the Scale for Assessment and Rating of Ataxia?

A

Evaluating truncal and extremity ataxia, gait ataxia and talking

128
Q

What are the purposes of the Ataxia Functional Composite Scale?

A

Evaluating gait speed, upper extremity ataxia and visual acuity

129
Q

What is the purpose of the Nine Hole Peg Test and the Computer Graphics Tablet?

A

Evaluating upper extremity ataxia

130
Q

What are the purposes of Friedreich’s ataxia impact scale?

A

Speech, upper limb functioning, lower limb functioning, body movement, complex tasks, isolation, mood, self perceptions.

131
Q

What is the purpose of the Composite cerebellar functional severity score?

A

Upper limb functions

132
Q

Describe features of hypotonicity associated w/ cerebellar dysfunctions

A

There is a decreased, pendulous myotatic reflex, as the decreased muscle resistance tends to cause the limb to swing back and forth after the initial reflex contraction.
disturbances and postural asymmetry. Hypotonia in the muscles of speech promotes abnormalities in pitch and loudness, and in oculomotor muscles results in difficulty in maintaining the gaze.

133
Q

Movement Decomposition

A

Inability to correctly sequence fine, coordinated acts

134
Q

What contributes to Gait Disturbance?

A

Decreased tone in postural muscles contributes to gait disturbances; gait disturbance is to be expected with practically all cerebellar lesions and by itself does little to localize the site of cerebellar damage.

135
Q

Treatments for cerebellar dysfunctions - motor, postural, and perceptual

A

PNF, rhythmic stabilization, slow reversal techniques, resistive exercises, Johnstone pressure splints, gt ex (on different surfaces) with EO and EC, plyometrics, balance board-ball, minitrampoline ex, vibration

136
Q

Give examples of interventions for motor learning and gait training for pts w/ cerebellar dysfunction. Also, describe recovery of function for these pts.

A

Motor learning: Ball tossing and Step over objects (to anticipate where they need to step).
Gait training: Have them use an assistive device to prevent their falling and just work on walking on different level surfaces.
Recovery of function: Varies if it is acquired or hereditary; Also varies depending on the severity of the disorder; Subacute ataxia: 6 months for full recovery.

137
Q

Important aspects to educate family on in regards to a pt w/ cerebellar dysfunction.

A

Pt is going to constantly need someone around since they are likely to fall due to their ataxic gait and the nystagmus.
Be aware of the patient having mood and mental changes.

138
Q

Respiratory function testing for myasthenia gravis

A

Examine for breathing difficulty or hoarse voice

139
Q

Physical Therapy goals for myasthenia gravis

A

Monitor changes in patient’s condition for complications, vital signs, respiration and swallowing; Promote independence in FMS and ADLs; Teach energy conservation techniques: activity pacing: promote optimal activity with rest as indicated

140
Q

Brain tumor: How many tumor grades exist?

A

4

141
Q

Radiation therapy

A

Uses high-energy beams, such as X-rays or can be focused on one specific location or the entire brain.

142
Q

Radiotherapy

A

Uses multiple beams of radiation to give a highly focused form protons, to kill tumor cells. (whole brain radiation) of radiation treatment to kill the tumor cells in a very small area.

143
Q

Chemotherapy

A

Use of drugs to kill the tumor cell; Taken orally or intravenously; Temodar is the most commonly used drug. Targeted Drug Therapy. Focus on specific abnormalities present within the cancer cells. Avastin is given intravenously and stops the formation of new blood vessels, cutting off the tumors blood supply.

144
Q

Factors that influences the prognosis of a patient diagnosed with a brain tumor:

A
  • Type and grade of tumor
  • Where the tumor is?
  • Is this a first occurrence or a recurrence of previous tumor
  • The general health of the patient
  • Whether the tumor can be removed by surgery. Is the patient a good candidate for surgery, or do they need other forms of treatment.
  • Has the tumor spread?
  • How well does the cancer respond to treatment?
  • Reports of survival greater that five years vary from less than 10% to a high of 32% no matter what treatment plan is used.
145
Q

T/F? Complete recovery from brain tumors rare.

A

True

146
Q

S&S of an abscess and how long are the symptoms present?

A

In almost all cases symptoms are present for less than 2 wks; Dependent on size and location of the lesion; Often present with fever, HA, and focal neurological deficits; Changes in mental status due to cerebral edema, nausea vomiting, neck stiffness

147
Q

Exam findings for an abscess include what?

A

ataxia, papilledema, general or focal seizures, drowsiness, hemiparesis, and slurred speech

148
Q

General Aspects of Patient Management for an abscess include what?

A

Strengthening, ROM, bed mobility and transfers, possible TMJ mobilization if a craniotomy is performed to remove abscess

149
Q

What to look for in the examination for encephalitis and what does the exam entail?

A

Look for sores around lips or genitals, mosquito bites, ticks. Complete neurologic exam, blood test, CT scan or MRI, spinal tap, brain biopsy.

150
Q

What percentage of people die from untreated herpes encephalitis within 18 months?

A

50%-75%

151
Q

Education of Family for encephalitis

A

Teach family how to help the transfer and ADLs, help with PROM to prevent contractures

152
Q

Diagnostic Tests for MS?

A 
LP/CSF,
elevated gamma globulin
CT or MRI
Myelogram
EEG
153
Q

What are some effects of Huntington’s Disease?

A

cognitive/emotional disturbances (executive function, visuospatial issues, dementia, personality changes)
voluntary/involuntary movement problems
trouble walking, speaking, swallowing
poor coordination
degeneration of caudate and putamen
dystonia, athetosis, akinesia, bradykinesia, chorea
Death due to respiratory issues

If onset is pre-age 20; seizures likely

154
Q

How is a patient with Huntington’s DIsease examined?

A
  • Bicaudate diameter: Measuring head of caudate nuclei
  • Genetic tests/family history
  • Neurological exam (touch, vision, hearing, coordination, balance)
  • Psychiatric exam
155
Q

Tool(s) assessing dynamic balance

A

Tandem Walking and Four Square Step Test

156
Q

Basal Ganglia Disease
Common Disorders - 3
Affect _ people in US

A
  • Parkinson’s, Huntington Chorea and dystonias (including drug induced dyskinesias)
  • affects 1 million people
157
Q

Speech language therapy for Huntington’s Disease

A

Training muscles involved in speech, eating, and swallowing

158
Q

Medications for Huntington’s Disease

A

Anticonvulsants, Benzodiazepines,, Antidepressants, Antipsychotics, Anti-seizure, Mood Stabilizers, and other medications for muscle disorders (dystonia, rigidity)

159
Q

Conditions that lead to BGD

A
  • carbon monoxide poisoning
  • copper poisoning
  • drug OD
  • head injury
  • infection
  • liver disease
  • metabolic problems
  • MS
  • medication side effects
  • stroke
  • tumors
160
Q

BGD Motor learning and recovery of function

A
  • use self generated movements that require feed forward control
  • pt. prefer sensory guided movements under feedback control - play key role in prediction or planning.
161
Q

Patients w/ Huntington’s Disease usually die within how many years?

A

15-20

162
Q

What are some impairments involved in Basal Ganglia Disease?

A
  • muscle tone
  • movement coordination and motor control
  • postural stability
  • presence of extraneous movement
163
Q

BGD Therapy examination and pt. management

A
  • posture
  • strength
  • flexibility
  • walking
  • balance
  • coordination
  • transferring in ADLS
  • fine motor movements ect.
164
Q

ALS changes…

A
  • eye, bowel and bladder muscles normally spared until terminal stages
  • 5% frontal/temporal dementria, normally cognitive function spared
  • hearing, sight, smell, touch, taste remain intact
  • Dysarthria, dysphagia, dysphonia secondary to pseudobulbar palsy and progressive bulbar palsy
165
Q

Death due to ALS

A

happens in 2-5 years

166
Q

General PT management of ALS

A
  • Pharmaceutical Therapy: Baclofen, Diazepan, Trihexyphenidyl, Amitrptyline
  • PT, OT, Speech to maintain functional abilities
  • Avoiding foods difficult to swallow
  • Respiratory Therapy
  • Breathing Devices
  • Homecare, social work, hospice
167
Q

Education of Family for ALS

A
  • prepare small meals throughout the day with enough calories
  • avoiding foods that may get caught in airway
  • airway clearance
  • breathing devices
  • safety in transfers
  • posture/wheelchair positioning
  • emotional support
  • skin checks
  • PROM
168
Q

Name 4 types of myasthenia gravis

A

Ocular myasthenia, Mild generalized myasthenia, Severe generalized myasthenia, Crisis

169
Q

Describe Myasthenic crisis

A

myasthenia gravis with respiratory failure; treat as medical emergency

170
Q

Cranial nerve testing for myasthenia gravis

A

Examine for diploplia, ptosis, progressive dysarthria or nasal speech, difficulty in chewing and swalling, difficulties in facial expression, drooping facial mm

171
Q

Functional mobility skills testing for myasthenia gravis

A

common difficulty with climbing stairs, rising from a chair or lifting

711 Adult Neurological Rehab (12 decks)

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