Neuro Pathology Flashcards

(66 cards)

1
Q

Meningitis

A

Bacterial: sicker, more rapid course; treat infective organism
OR
Viral: treat with antibacterial therapy (antibiotic, antipyretic) and maintain fluid/electrolyte balance

Provide supportive symptomatic therapy
Bed positioning, PROM, skin care, safety measures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Encephalitis

A

Severe infection and inflammation of the brain
Caused by arboviruses or a sequela of influenza, chronic and recurrent sinusitis, otitis, or other infections; bacterial encephalitis, prioncaused disease (“mad cow”)

Treat infective organism (bacterial encephalitis)

Provide supportive symptomatic therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Brain abscess

A

Infectious process in which there is a collection of pyogenic material in the brain parenchyma

S/S: H/A, fever, brainstem compression, focal signs CN II and VI

Can be an extension of an infection, typically frontal or temporal lobes or cerebellum

Treat infective organism, surgical intervention
Provide supportive symptomatic therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Acquired immunodeficiency syndrome (AIDS)

A

Viral syndrome characterized by acquired and severe depression of cell-mediated immunity

S/S: wide ranging, 1/3 exhibit CNS/PNS deficits

  • AIDS dementia complex (ADC): range from confusion to memory loss to disorientation
  • Motor deficits: ataxia, weakness, tremor, loss of fine motor coordination
  • Peripheral neuropathy: hypersensitivity, pain,s sensory loss

Treat with anti-HIV drugs
Provide palliative and supportive therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
Cerebrovascular Accident (CVA) 
(PT GOALS only)
A
ROM and prevent deformity
Skin integrity
Sensory compensation strategies
Strengthen all available muscles
Normalize of tone
Selective movement control (out of synergy)
Postural control, balance and symmetry
Task-specific training
Respiratory and oromotor control
Isokinetic training
Locomotor training with body weight support 
Biofeedback training
Constraint-Induced movement therapy (CIMT)

DO NOT:
Use overhead pulleys on hemiplegic UE (traction injury risk)
Prescribe exercise/progressive physical activity without monitoring HR/BP
Use CIMT if pt doesn’t meet minimal movement criteria at wrist and fingers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Traumatic Brain Injury (TBI)

MOI
Concussion

A

MOI is contact forces to skull and rotational acceleration forces, causing varying degrees of injury to brain

Concussion: LOC either temporary or permanent resulting from injury or blow to head with impaired functioning of RAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

TBI: PRIMARY BRAIN DAMAGE

A

Primary brain damage (types of injuries):

(1) Diffuse Axonal: disruption/tearing of axons and small blood vessels from shear-strain of angular acceleration leading to neuronal death and petechial hemorrhages
(2) Focal: contusions, lacerations, mass effect from hemorrhage and edema
(3) Coup-Contracoup: injury at point of impact and opposite point of impact
(4) Closed or Open: fracture of skull

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

TBI: SECONDARY BRAIN DAMAGE

A

Secondary brain damage:

(1) Hypoxic-ischemic: systemic problems (respiratory or cardiovascular) that compromise cerebral circulation
(2) Swelling/edema: mass effect with increased ICP, brain herniation and death
(3) Electrolyte imbalance: mass release of damaging neurotransmitters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

TBI DEFINITIONS

COMA

A

State of unconsciousness in which there is neither arousal nor awareness
Eyes remain closed, No sleep/wake cycles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

TBI DEFINITIONS

UNRESPONSIVE VIGILIANCE/VEGETATIVE STATE

A

Marked by the return of sleep/wake cycles and normalization of vegetative functions (respiration, digestion, BP control)
Persistent vegetative state: vegetative state >1 year post TBI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

TBI DEFINITIONS

MUTE RESPONSIVENESS/MINIMALLY RESPONSIVE

A

State in which patient is not vegetative and does show signs, even if intermittent, of fluctuating awareness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

TBI DEFINITIONS

CONFUSIONAL STATE

A

Mainly a disturbance of attention mechanisms
All cognitive operations are affected, patient is unable to form new memories
May demonstrate either hypoarousal or hyperarousal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

TBI DEFINITIONS

EMERGING INDEPENDENCE

A

Confusion is clearing and some memory is possible
Significant cognitive problems and limited insight remain
Frequently uninhibited social behaviors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

TBI DEFINITIONS

INTELLECTUAL/SOCIAL COMPETENCE

A

Increasing independence, although cognitive difficulties (problem solving, reasoning) persist along with behavioral and social problems (enhancement of premorbid traits, mood swings)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

TBI

PT GOALS FOR RANCHOS LOS AMIGOS LEVELS OF COGNITIVE FUNCTIONING (LOCF) I-III

(5)

A

(1) Maintain ROM, prevent contracture development: PROM, positioning, splinting and serial casting
(2) Maintain skin integrity, prevent decubitus ulcers through frequent position changes
(3) Maintain respiratory status, prevent complications: PD, percussion, vibration, suctioning to keep airway clear
(4) Sensory stimulation for arousal and to elicit movement: environmental/direct stimulation
(5) Promote early return of FMS: upright positioning and proper body alignment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

TBI

PT GOALS FOR RANCHOS LOS AMIGOS LEVELS OF COGNITIVE FUNCTIONING (LOCF) IV-VI

(7)

A

(1) Structure and prevent overstimulation for confused, agitated patient: closed, reduced stimulus environments, daily logs, relaxation
(2) Provide consistency: team-determined behavioral modification techniques, clear feedback, written contacts
(3) Task-specific training: familiar and well-liked activities, off options, break down complex task
(4) Verbal or physical assistance
(5) Control rate of instruction, frequent orientation to time, place, etc.
(6) Safety, behavioral management
(7) Model calm, focused behavior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

TBI

PT GOALS FOR RANCHOS LOS AMIGOS LEVELS OF COGNITIVE FUNCTIONING (LOCF) VII-VIII

(5)

A

(1) Increasing independence
(2) Assist in behavioral, cognitive, emotional reintegration: honest feedback, prepare for community re-entry
(3) Independence in functional tasks: FMS, ADLs, real-life environments
(4) Improve postural control, symmetry and balance
(5) Active lifestyle, improve endurance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

SPINAL CORD INJURY

CENTRAL CORD SYNDROME

A

Loss of more centrally located cervical tracts/arm function with preservation of more peripherally located lumbar and sacral tracts/leg function
Typically caused by hyperextension of cervical spine

Loss of spinothalamaic tracts: B pain/temp
Loss of ventral horn: B motor function (UE)
Preservation of proprioception and discriminatory sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

SPINAL CORD INJURY

BROWN-SEQUARD SYNDROME

A

Hemisection of spinal cord typically caused by penetration wounds (gunshot or knife) with asymmetrical symptoms

IPSI loss of dorsal col: tactile discrim, pressure, vibration and proprioception
IPSI loss of corticospinal: motor function and spastic paralysis below level of lesion
CONTRA loss of spinothalamic: pain/temp below level and B pain/temp loss at level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

SPINAL CORD INJURY

ANTERIOR CORD SYNDROME

A

Damage mainly in anterior cord leading to loss of motor function, pain and temperature with preservation of light touch, proprioception and position sense
Typically caused by flexion injuries of cervical spine

Loss of lateral corticospinal: motor function and spastic paralysis below level
Loss of spinothalamic: B loss pain/temp
Preservation of dorsal col: proprio, kinesthesia and vibratory sense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

SPINAL CORD INJURY

POSTERIOR CORD SYNDROME

A

Loss of posterior columns with preservation of motor function, sense of pain and light touch; extremely rare

Loss of dorsal col B
B loss proprioception, vibration, pressure, and epicritic sensations (stereognosis, 2pt discrim)
Preservation of motor function, pain and light touch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

SPINAL CORD INJURY

CAUDA EQUINA

A

Injury below L1 results in injury to lumbar and sacral roots of peripheral nerves (LMN) with sensory loss and paralysis and some capacity for regeneration
A LMN lesion with autonomous or nonreflex bladder

Flaccid paralysis with no spinal reflex activity
Flaccid paralysis of bowel and bladder
Potential for nerve regeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

SPINAL CORD INJURY

SACRAL SPARING

A

Sparing of tracts to sacral segments with preservation of perianal sensation, rectal sphincter tone or active toe flexion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

SPINAL CORD INJURY

CHANGES TO MONITOR FOR (5)

A

(1) Spinal Shock: transient period of reflex depression/spasticity, up to 24 weeks
(2) Spasticity/Spasms: location of tone, examine nociceptive stimuli that trigger incr tone
(3) **Autonomic Dysreflexia: emergency situation in which noxious stimulus precipitates pathological autonomic reflex
- Leads to bradycardia, H/A, diaphoresis, flushing, diplopia, or convulsions
- Examine for irritating stimuli
- ELEVATE head, check/empty catheter FIRST
(4) Heterotopic bone formation: abnormal bone growth in soft tissues; soft tissue swelling, pain, erythema–generally near large joints
(5) Deep venous thrombosis: edema and tenderness in LE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
SPINAL CORD INJURY PT GOALS
``` Respiratory capacity: deep breathing, strengthening, assisted coughing, respiratory hygiene, abdominal support Maintain ROM, prevent contracture Maintain skin integrity, free of decubitus ulcers and injuries Improve strength Reorient patient to vertical position Promote early return of FMS and ADLs Improve sitting tolerance Cardiovascular endurance ```
26
SPINAL CORD INJURY WHEELCHAIR PRESCRIPTION: C1-4
Electric wheelchair with tilt-in-space seating or reclining seat back Microswitch or puff-and-sip controls Portable respirator may be attached
27
SPINAL CORD INJURY WHEELCHAIR PRESCRIPTION: C5
Manual wheelchair with propulsion aids Independent for short distances on smooth, flat surfaces May choose electric wheelchair for distance and energy conservation
28
SPINAL CORD INJURY WHEELCHAIR PRESCRIPTION: C6
Manual wheelchair with friction surface hand rims | Independent
29
SPINAL CORD INJURY WHEELCHAIR PRESCRIPTION: C7
Manual wheelchair with friction surface hand rims with increased propulsion ability Independent
30
SPINAL CORD INJURY WHEELCHAIR PRESCRIPTION: C8-T1 AND BELOW
Manual wheelchair, standard hand rims
31
LOCOMOTOR TRAINING FOR INDIVIDUALS WITH COMPLETE INJURIES: T6-9
Supervised ambulation for short distances requires bilateral KAFO's and crutches Swing-to gait pattern Requires assistance May prefer standing devices/wheelchairs for physiological standing
32
LOCOMOTOR TRAINING FOR INDIVIDUALS WITH COMPLETE INJURIES: T12-L3
Independent in ambulation on all surfaces and stairs using a swing-through or four point gait pattern and bilateral KAFO's and crutches May use RGOs with walker with or without FES system Independent household ambulators, wheelchair use for community ambulation
33
LOCOMOTOR TRAINING FOR INDIVIDUALS WITH COMPLETE INJURIES: L4-5
Independent with bilateral AFO's and crutches or canes Typically independent community ambulatory May use wheelchair for activities with high-endurance requirements
34
SPINAL CORD INJURY ABSOLUTE CONTRAINDICATIONS TO EXERCISE TESTING
``` Autonomic dysreflexia Severe/infected skin on WB surfaces Symptomatic hypotension UTI Unstable fracture Uncontrolled hot/humid environment Insufficient ROM to complete exercise ```
35
LOCOMOTOR TRAINING FOR INDIVIDUALS WITH INCOMPLETE INJURY
Treadmill Training (TT) with body weight support (BWS) Incomplete injuries (ASIA B, C and D) Variable levels of loading: 35% to 10% to full High frequency (4 days/wk) Moderate duration (20-30 min) 8-12 weeks
36
Multiple Sclerosis Characteristics
Chronic, progressive, demyelinating disease of the CNS affecting mostly young adults Demyelinating lesions (plaques) impair neural transmission causing nerves to fatigue rapidly Variable symptoms: lesions scattered in time and place, lesions common in pyramidal tract, dorsal columns and periventricular areas of cerebrum, cerebellar peduncles Variable course with fluctuating periods Precipitating or exacerbating factors: infections, trauma, pregnancy, stress Transient worsening of symptoms: adverse reactions to heat, hyperventilation, dehydration and fatigue
37
Relapsing-remitting MS (RRMS)
Relapses with either full recovery or some remaining neurological S/S and residual deficit on recovery; periods between relapses characterize by lack of disease progression
38
Primary-progressive MS (PPMS)
Disease progression from onset without plateaus or remissions or with occasional plateaus and temporary minor improvemnts
39
Secondary-progressive MS (SPMS)
Initial relapsing-remitting course followed by progression at a variable rate that may also include occasional relapses and minor remissions
40
Progressive-relapsing MS (PRMS)
Progressive disease from onset but without clear, acute relapses that may or may not have some recovery or remission Commonly seen in individuals who develop disease after 40 years old
41
Multiple Sclerosis Medical Management PT GOALS
Med Management: (1) Immunosuppressant drugs (ACTH, steroids) (2) Interferon drugs (Avonex, Betaseron, Copaxone) (3) Symptomatic management of spasticity (drugs, baclofen pump, phenol block surgery) (4) Symptomatic management of urniary problems (anticholinergic drugs) ``` PT GOALS: Monitor changes: UTI, respiratory infection Restorative: intensive, time-limited Functional maintenance ROM, prevent contractors Skin integrity Sensory awareness Strength Motor control coordination Postural control, symmetry, balance Independence with mobility and ADLs Energy conservation techniques ``` AVOID Precipitating exacerbations: schedule PT during optimal times for function Overheating Stressors
42
Parkinson's Disease Characteristics Stages
Chronic, progressive disease of CNS with degeneration of dopaminergic substantia nigra neurons and nigrostriatal pathways Deficiency of dopamine within basal ganglia corpus striatum with degeneration of substantial nigra Loss of inhibitory dopamine results in excessive excitatory output from cholinergic system (acetylcholine) of basal ganglia Rigidity (leadpipe or cogwheel) Bradyinesia Resting tremor Impaired postural reflexes STAGES I: minimal or absent disability, unilateral Sx II: minimal B or midline involvement, NO balance involvement III: all sx present and severe; stands and walks only with assistance IV: confinement to bed/wheelchair
43
Parkinson's Disease Medical Management PT GOALS
Med Management: (1) Sinemet (levdopa/carbidopa): provides dopamine and decreases effects of disease; effect is prolonged with low-protein diet; in on-off phenomenon: sudden changes from normal function to immobility to severe dyskinetic movement (2) Dopamine agonist drugs: enhance effects of Sinemet therapy (3) Anticholinergic drugs: control tremors (4) Amantadine: enhances dopamine release (5) Selegiline (deprenyl): monoamine oxidase inhibitor increases dopamine; used early in disease to slow progression (6) Deep brain stimulation in thalamus or sub thalamic nucleus ``` PT GOALS: Monitor changes Prevent/minimize secondary impairments Compensatory strategies: initiate movement, repetitive auditory stimulation Improve strength Relaxation skills Postural control, symmetry, balance Improve gait, locomotor training Independence in FMS and ADLs Maximum mobility and safety ```
44
Myasthenia gravis
Neuromuscular junction disorder characterized by progressive muscular weakness and fatiguability on exertion Muscular strength worse with continuing contraction, improved with rest 4 types: ocular myasthenia (confined to extraocular mm) mild generalized myasthenia severe generalized myasthenia crisis -Generalized: bulbar (extraocular, facial and muscles of mastication) and proximal limb-girdle mm May progress form mild to severe within 18 months EXAMINE cranial nerves respiratory function mm strength: proximal more involved, fatigue functional mobility: climb stairs, sit to stand, lifting EMG and repetitive nerve stimulation: slow abnormal responses ``` MED MANAGEMENT: acetylcholinesterase inhibitors corticosteroids immunosuppressants alternative: plasmapheresis, thymectomy ``` PT GOALS: changes in condition: vitals, respiration, swallowing energy conservation
45
Epilepsy Symptoms Causes
Disorder characterized by recurrent seizures (repetitive abnormal electrical discharges within the brain) ``` Symptoms: altered consciousness altered motor activity (convulsion): involuntary mm contraction, tonic (stiff/rigid) and clonic (rhythmic jerking) sensory phenomena autonomic phenomena cognitive phenomena ``` Causes: acquired brain disease or trauma: tumor, stroke degenerative brain disease: alzheimers, amyloidosis developmental brain defects drug overdose/withdrawal electrolyte disorders hyperthermia infections, brain abscess, meningitis, neurocysticerocosis pregnancy complications
46
Epilepsy Classification of Generalized Seizures
Tonic-Clonic (Grand Mal): dramatic loss of consciousness, with a cry, fall and tonic-clonic convulsions of all extremities - tongue biting and arrested breathing, incontinence - contractions subside after 2-5 min and consciousness is gradually regained - pt is confused, drowsy and amnesiac after event - full recovery may take several hours Absence Seizures (Petit-Mal): brief, almost imperceptible lapse of consciousness followed by immediate and full return to consciousness - posture is maintained with no convulsive muscle contractions - may occur 100x/day
47
Epilepsy Classification of Partial Seizures
Simple Partial Seizures: focal, begin locally limited to a portion of the body, consciousness preserved; usually has an identified structured cause Focal Motor: clonic activity involving a specific area of the body Focal Motor with March (Jacksonian): orderly spread or march of clonic movements from initial muscles to involve adjacent muscles, with spread to entire side Temporal Lobe Seizure: episodic changes in behavior with complex hallucinations, automatisms (lip smacking, chewing, etc.), altered cognitive and emotional function, preceded by an aura
48
Epilepsy Secondarily generalized seizures Status epilepticus
Secondary generalized seizures: simple or complex partial seizures evolving to a generalized seizure Status epilepticus: prolonged seizure or a series of seizures (>30 min) with very little recovery between attacks; may be life threatening medical emergency
49
Epilepsy Medical Management PT GOALS
Med Management: Antiepileptic meds: phenytoin (Dilantin), carbamazepine (Tegretol), phenobarbital Surgical: lobe resection, hemispherectomy PT GOALS: Protect pt from injury Establish airway, prevent aspiration
50
Lesions of archicerebellum, paleocerebellum and neocerebellum
LESIONS OF CEREBELLUM = IPSI S/S Archicerebellum: - central vestibular sx: ocular dysmetria, poor eye pursuit, dysfunctional VOR, impaired eye-hand coordination - gait and trunk ataxia - little change in tone or dyssynergia of extremity movements Paleocerebellum: - hypotonia - truncal ataxia - ataxic gait Neocerebellum: - intention tremor - dysdiadochokinesia - dysmetria - dyssynergia Additional impairments: asthenia, hypotonia, motor learning impairments, cognition, emotional dysregulation PT GOALS: improve accuracy of limb movement, postural stability, functional mobility, VOR
51
Unilateral vestibular disorders (UVD)
Trauma: vestibular symptoms in 30-65% of patients with TBI Vestibular neuronitis, labyrinthitis: acute infection with prolonged attack of sx, persisting for several days/weeks caused by viral/bacterial infection Menieres disease: recurrent, usually progressive; episodic attacks may last from minutes to several hours with severe sx; assoc with tinnitus, deafness, sensation of pressure/fullness in ear; edema of membranous labyrinth Benign paroxysmal positional vertigo (BPPV): brief attacks of vertigo/nystagmus that occur with certain head positions; may be related to degenerative processes, mechanical impairment of peripheral vestibular system Tumor: acoustic neuroma, gliomas/brainstem or cerebellar medulloblastoma Medical management: vestibular suppressant medications PT GOALS: safety measures habituation training: repetition of mvoements/postures that provoke dizziness and verge gaze stability exercises: eye movements (X1/X2), head movements postural stability: sitting, standing, dynamic balance relaxation training BPPV: canalith repositioning treatment (CRT)--horizontal and posterior SCC BPPV liberatory maneuver--posterior SCC BPPV brandt-daroff exercises--residual/mild vertigo
52
Bilateral vestibular disorders (BVD)
Toxicity: ototoxic drugs Bilateral infection: neuritis, meningitis Vestibular neuropathy, otosclerosis (Paget's disease) Medical management: vestibular suppressant medications PT GOALS: safety measures habituation training: repetition of mvoements/postures that provoke dizziness and verge gaze stability exercises: eye movements (X1/X2), head movements postural stability: sitting, standing, dynamic balance relaxation training
53
Peripheral nerve disease/injury Wallerian degeneration
Transection (neurotmesis) results in degeneration of axon and myelin sheath distal to site - chromatolysis and repair process in nerve cell body - endoneurium (sheath) does NOT degenerate but forms a tube directing regeneration
54
Peripheral nerve disease/injury Segmental demyelination
axons are preserved; demyelination restores function
55
Peripheral nerve disease/injury Axonal degeneration
degeneration of axon cylinder and myelin, distal to proximal
56
Peripheral nerve disease/injury Neuropathy Radiculopathy
Neuropathy: disease of nerves characterize by deteriorating neural function Polyneuropathy: B symmetrical involvement of peripheral nerves, LE>UE, distal earlier and more involved proximal Mononeuropathy: involvement of a single nerve Radiculopathy: involvement of nerve roots
57
Peripheral nerve diease/injury Traumatic nerve injury classes
Neurapraxia (Class 1): injury to nerve that causes a transient loss of function (conduction block ischemia); nerve dysfunction may be rapidly reversed or persist a few weeks (compression) Axonotmesis (Class 2): injury to nerve interrupting the axon and causing loss of function and wallerian degeneration distal to the lesion; with no disruption of the endoneurium, regeneration possible (crush injury) Neurotmesis (Class 3): cutting of the nerve with severance of all structures and complete loss of function; rein nervation typically fails without surgical intervention because of aberrant regeneration (failure of regenerating axon to find its terminal end
58
Clinical symptoms of LMN syndrome and Diagnostic tests
Weakness/paresis of denervated muscle, hyporeflexia and hypotonia, (rapid) atrophy, fatigue Sensory loss: corresponds to motor weakness; proprioceptive losses may yield sensory ataxia; insensitivity may yield limb trauma Autonomic dysfunction: vasodilation and loss of vasomotor tone (dryness, warm skin, edema, orthostatic hypotension) Hyper excitability of remaining nerve fibers - Sensory dyesthesias: hyperalgesia, pins and needles, N/T, burning - Motor: fasciculations, spasms Muscle pain (myalgia) with inflammatory myopathies Diagnostic tests: NCV=slowed conduction times or complete conduction block may be evident EMG=signs of denervation atrophy (spontaneous fibrillation potentials); evidence of reinnervation (low-amplitude, short duration, polyphasic motor unit potentials)
59
Trigeminal neuralgia
Neuralgia of trigeminal nerve (CN V) results from degeneration or compression (tortuous basilar artery or cerebellopontine tumor) occurs in older pop. (mean age 50 y/o), abrupt onset Brief paroxysms of neurogenic pain (stabbing and/or shooting) reoccurring frequently - along distribution of trigeminal nerve, mandibular and maxillary divisions, restricted to ONE SIDE of the face - autonomic instability: exacerbated by stress, cold; relieved by relaxation Medical management: medications (anti-convulsants, vitamin B12), alcohol injections, surgery TENS may be effective for pain relief
60
Bell's palsy | Facial paralysis
LMN lesion involving CN VII (facial nerve) resulting in UNILATERAL facial paralysis Acute inflammatory process of unknown etiology (immune or viral) resulting in compression of the nerve within the temporal bone Characteristics: (1) mm of facial expression on one side are weakened or paralyzed (2) loss of control of salivation or lacrimination (3) onset actue, with max severity in a few hours or days, commonly preceded by a day or two of pain behind ear; most recover in several weeks or months (4) sensation is normal Meds: corticosteroids, analgesics PT GOALS: protect cornea (artificial tears or patching) e-stim to maintain tone active facial exercises sling to prevent overstitching of facial mm functional retraining
61
Bulbar palsy | bulbar paralysis
Weakness or paralysis of muscles innervated by motor nuclei of the lower brainstem, affecting mm of face, tongue, larynx and pharynx Result of tumors, vascular or degenerative diseases of lower cranial nerve motor nuclei EXAMINE: Glossopharyngeal and vagal paralysis: phonation, articulation, palatal action, gag reflex, swallowing Voice quality B involvement: airway restriction Psuedobulbar palsy: B dysfunction of corticobulbar innervation of brainstem uncle; central or UMN lesion analogous to corticospinal lesions disrupting function of anterior horn cells -Examine for hyperactive reflexes: increased jaw jerk and snout reflex PT GOALS: suctioning, oral care maintain respiratory function elevate head of bed
62
Guillain-Barre syndrome
Polyneuritis with progressive muscular weakness with an autoimmune attack, usually occurs after recovery from an infections disease (respiratory or GI) Characteristics: (1) Acute demyelination of both cranial and peripheral nerves (LMN disease) (2) Sensory loss, paresthesisas (tingling, burning) pain; less than motor loss (3) Motor paresis/paralysis: symmetrical distribution of weakness; LE to UE and distal to proximal (4) Dysarthria, dysphagia, diplopia and facial weakness (5) Progression evolves over a few wks/days recovery usually slow (6 mo to 2 yrs) and usually complete ``` COMPLICATIONS: Respiratory impairment/failure Autonomic instability Pain Risk of pneumonia Prolonged hospitalizations/immoblity Relapse ``` Medical: good nursing care, plasmapheresis, IVIG, analgesics ``` PT GOALS: maintain respiratory function prevent indirect impairments: PROM, positioning, skin care prevent injury to denervated muscles muscle re-educatoin energy conservation ```
63
Amyotrophic lateral sclerosis (ALS, Lou Gehrig's Disease) Description Characteristics
Degenerative disease affecting UMNs and LMNs (degeneration of anterior horn cells and descending corticobulbar and corticospinal tracts) Characteristics: (1) Progressive, often leading to death in 2-5 years - Bulbar onset: progressive bulbar palsy - Spinal cord onset: progressive mm atrophy (2) Muscular weakness that spreads over time limbs to body; mm fasciculations or twitching (LMN signs) (3) Spasticity, hyperreflexia (UMN signs) (4) Dysarthria, dysphagia, dysphonia (5) Absence of sensory changes (6) Autonomic dysfunction (1/3 pts) (7) Pain due to spasticity, cramping, postural stress syndrome, hypo mobility or instability (8) Respiratory impairments: weakness (9) Sparing of bowel/bladder function (10) Depression common
64
Amyotrophic lateral sclerosis (ALS, Lou Gehrig's Disease) Stages (6)
Stage I: Early disease, mild focal weakness, asymmetrical distribution, symptoms of hand cramping and fasciculations Stage II: moderate weakness in groups of mm, some wasting (atrophy) of mm; modified independence with assistive devices Stage III: severe weakness of specific mm, increasing fatigue; mild to moderate functional limitations, ambulatory Stage IV: severe weakness and wasting of Les, mild weakness of UEs, moderate assistance and assistive devices required; wheelchair user Stage V: progressive weakness and deterioration of mobility and endurance, increased fatigue, moderate to severe weakness of whole limbs and trunk; spasticity, hyperreflexia; loss of head control; maximal assistance Stage VI: bedridden, dependent ADLs, FMS; progressive respiratory distress
65
Amyotrophic lateral sclerosis (ALS, Lou Gehrig's Disease) Examination Medical management PT GOALS
``` Examine: Cranial Nerves VII, IX, X, XI, XII Motor function: symmetrical distribution Spasticity, hyperreflexia ALS Functional Rating Scale (ALSFRS) ``` Medical management: no effective tx; Riluzole (glutamate antagonist) slows progression, symptomatic relief PT GOALS: respiratory function nutritional needs indirect impairments: PRM, positioning, skin care moderate exercise program (monitor fatigue) energy conservation family/caregiver education
66
Postpolio syndrome (PPS)
New slowly progressive muscle weakness occurring in individuals with confirmed history of acute poliomyelitis due to possible hyper functioning of motor neurons, one term overuse at high levels resulting in new denervation Characteristics: (1) new weakness/atrophy; ASYMMETRICAL (2) abnormal fatigue (3) pain (4) decreased function with reduced endurance (5) slow progression: steady or stepwise (6) environmental cold intolerance (7) difficulty concentrating, memory, attention: damage to reticular formation, hypothalamus, dopaminergic neurons (8) sleep disturbances (9) decreased functional mobility Examine: motor function: spotty involvement, asymmetrical EMG to identify prior anterior horn cell disease and new motor unit pathology Medical management: antidepressants, neurotransmitter inhibitors PT GOALS: maintain respiratory function energy conservation (avoid unnecessary activities to maximize important work) preserve/increase muscle strength (mod exercise program) aerobic conditioning (mod to low level) orthoses, mobility aids, assistive devices