Ryan Joseph M.

Dela Paz, PTRP, PT

UMNL:
 Huntington’s Disease
 Alzheimer’s Disease
 Seizures and Epilepsy

COMBINED UMN & LMN:

 Amyotrophic Lateral Sclerosis

LMNL
 Poliomyelitis & Post-polio syndrome
 Myasthenia Gravis
 Lambert-Eaton Myasthenic Syndrome
 Guillain Barre Syndrome
 Peripheral nerve injuries
 Abnormal gene HUNTINGTIN Ch. 4p16.3
 Neuronal atrophy of neostriatum –caudate &
putamen
 Also marked neuronal loss in cerebral cortex
 Varying degrees of atrophy in other parts of the
brain
Involuntary movements Behavioral changes
 Chorea  Behavioral
 Facial movements, disturbances
including grimaces  Hallucinations
 Slow, uncontrolled  Irritability
movements  Moodiness
 Unsteady gait  Restlessness or
Dementia fidgeting
 Disorientation or  Paranoia
confusion  Psychosis
 Loss of judgment
 Loss of memory
 Personality changes
 Speech changes
 No single imaging technique
 Measurement of bicaudatediameter by CT
scan or MRI is a reliable marker of HD
 Genetic testing
 No cure
 PT Goal: help patient maintain function for as
long as possible
 Dementia
 Insiduously progressive memory loss
 Behavioral changes
 Language disorders
 Impairment in visuospatialskills and executive
functions
Stage 1:
 lasts 2-4 years; loss of functional skills/orientation,
memory loss,lackof spontaneity. Depression is
common.
Stage 2:
 progressive memory loss & variety of neurological
sx; aphasias, apraxias, wandering, repetitive,
movements, wide-based gait, psychotic behaviors,
sundowning
Stage 3:
 vegetative symptoms; mute, stop eating, bowel &
bladder incontinence, inability to walk, seizures
 Only definitive diagnosis: autopsy
 PT:
 Patient history
 Mini Mental Status Examination
Treatment for mild to moderate AD
1.Cholinesterase inhibitors (ChEIs)
Donepezil (Aricept)
Galantamine (Razadyne)
Rivastigmine (Exelon)
2.Mental exercises
Can occur as a Also associated with
complication of  Febrile state
 CVA  Hypoxia
 Head trauma  Hyper/hypoglycemia
 Meningitis  Hyponatremia
 Surgery  Severe uremic/hepatic
encephalopathy
 Drug overdose
 Drug/alcohol
withdrawal
CLASSIFICATION CHARACTERISTICS

Simple motor -jerking, muscle rigidity, spasms, head-

turning
Simple partial Simple sensory -Unusual sensations affecting either the
vision, hearing, smell taste, or touch
Simple psychological -Memory or emotional
disturbances

Complex partial (+) automatisms

Partial with initially associated with a preservation of consciousness

secondary that then evolves into a loss of consciousness and
generalization convulsions
CLASSIFICATION CHARACTERISTICS

Tonic Muscle stiffness, rigidity

Tonic-clonic combination of tonic and clonic

Clonic Repetitive, jerking movements

Atonic Loss of muscle tone

Absence Brief loss of consciousness

Myoclonic Sporadic (isolated), jerking movements

Status epilepticus > 30mins

1) CARBAMAZEPINE
S/E:
drowsiness,dizziness,unsteadiness,nausea,vomiting,h
eadache,anxiety,memory problems, diarrhea,
constipation, heartburn ,dry mouth, back pain

**Some side effects can be serious. If you experience any

of these symptoms or those listed in the IMPORTANT
WARNING section, call your doctor immediately:
 confusion
 loss of contact with reality
 chest pain
 yellowing of the skin or eyes
 vision problems
 2) GABAPENTIN
 S/E: dizziness, fatigue, weight gain,
drowsiness, andperipheral edema
 PT consideration: weakness: utilize low
intensity of exercise especially when there are
obvious signs of side effects
 Stay with the person and guide gently aware from
or prevent access to dangerous areas
 Do not place anything in the person’s mouth
 Move objects away from the person to prevent
injury
 Only move the person if in an unsafe areas such as
a roadway or stairwell
 If in water, keep the person’s head above the water
 Don’t restrain the person’s movements
 Pad under the person’s head, arms and legs
 Keep track of how long the seizure lasts
*Recovery position: side-lying
CALL EMERGENCY IF:
 Two or more seizures occur without full recovery
of responsiveness between seizures (unless the
seizure protocol directs otherwise)
 When breathing does not resume after a seizure
start rescue breathing
 When this is the person’s first seizure
 When the person may have aspirated (seizure
occurs during eating, bathing, swimming, etc)
 When a seizure lasts for more than 5 minutes
(unless the seizure protocol directs otherwise)
 When the person cannot be aroused two hours
after the seizure (unless their protocol directs
otherwise)
 Amyotrophic lateral sclerosis is characterized
by a progressive degeneration and loss of
motor neurons in the spinal cord, brainstem,
and motor cortex
 First signs: asymmetric atrophy, weakness and
fasciculations
 UMN: mm weakness, spasticity, pathological
reflexes, hyperreflexia
 LMN: mm weakness, hyporeflexia,
hypotonicity, atrophy, fasciculations
 Bulbar pathology
 Respiratory impairments
Orthopnea, dyspnea, weak cough, decreased VC

 Cognitive impairments

 Indirect impairments:
Fatigue, weight loss, gait disturbances, deconditioning,
anxiety depression
 PHASES STAGE CHARACTERISTICS

I Mild focal weakness, asymmetrical, hand

cramping & fasciculations

Phase I II Mod weakness in mm group, modified

Independent independence
III Severe weakness of specific mm, high fatigue,
ambulatory with assistivedevice
Phase II IV Severe weakness & wasting of LE, mild UE, W/C
Partially user
independent V Deterioration of mobility, mod-severe wknessof
limbs & trunk, spasticity, max assist
Phase III VI Bedridden, respiratory distress
Dependent
 DIAGNOSIS INVOLVEMENT

I - suspected ALS UMN or LMN in ≥ 1 region

II-possible ALS UMN + LMN sign in 1 region

III-clinically UMN + LMN sign in 2 regions

probable

IV-clinically UMN + LMN sign in 3 regions

definite
Poor:
 Age at onset: >35-40 y.o

 Severe dse at onset: (+) dyspnea

 Bulbar onset

 female
Primary goal: assist pt in maintenance of fxn,
independence and quality of life as long as
possible
Drug therapy: NO CURE
 Riluzole –glutamate inhibitor-may slow
progression.
 50mg tablet 2x per day

 S/E: liver toxicity, asthenia, nausea, vomiting

and dizziness
 energy conservation techniques
 activity pacing
 splinting to prevent contractures
 ROM exercises
utilization of PNF patterns & techniques
 stretching exercises
 strengthening exercises
 pool therapy
 breathing exercises
 LIGHT endurance exercises
 pain management
1)Acute (1-6wks)
 -fever with peak at 3rd day (7-10 days)

 -HA, GIT symptoms, muscle stiffness & pain

 PARALYSIS
 LE: TA, peroneals, quads, gluteals
 UE: deltoids
 cold intolerance

*Cardinal sign: asymmetric weakness (LE)

 2) Convalescent/ Recovery Stage (6wks-
6months)
 -Recovery of strength monitored within 6 wks

 3)Residual / Chronic stage(>6mos)

 -weakness, atrophy, limb shortening, postural
and gait deformity
Clinically suspected in persons with acute onset
flaccid paralysis, (-) DTR that cannot be
attributed to another apparent cause, (-)
sensory and cognitive loss
 Stool sample or swab of pharynx

 Blood test: (+) antibodies for polio virus

 CSF: incWBC and mildly elevated proteins

 SALK
 SABIN
 a condition that affects polio survivors years
after recovery from an initial acute attack of the
poliomyelitis virus.
1. Confirmed history
2. Recovery
3. Stability
4. 2 or more of the criteria
 unaccustomed fatigue
 mm or joint pain
 new weakness in mm previously affected & unaffected
 functional loss
 cold intolerance
 new atrophy
 no other medical diagnosis to explain these health
problems
 MYASTHENIA GRAVIS LAMBERT EATON MYASTHENIC
SYNDROME
Post synaptic Pre-synaptic

Decreased ACH receptors Decreased ACH

Decrementing Increasing

Initially with strength, then decrease 2nd wind (Lambert sign)

Thymoma Bronchial Carcinoma

F>M M>F
a.HALLMARK: PEMS a. weakness of proximal LE mm
b.Bulbar involvement 1stthen UE
b. fatigue
-slurred speech with nasal twang c. dry mouth
-possible dysphagia & facial mm d. sexual dysfunction
paresis involvement (myasthenicsnarl) e. areflexia
-(+) diplopia & ptosis f. occasional bulbar signs (ocular mm)

MYASTHENIC CRISIS*
Edrophonium/ Tensilon test
 Use edrophonium chloride
(anticholinesterase) to stop breakdown of Ach
 If improves: myastheniccrisis

 If worsens: cholinergic crisis

 Atropine: control side effects of edrophonium

 Bradycardia, sweating and cramping
 distal & symmetrical motor weakness
 areflexia
 bilateral facial weakness
 respiratory mm paralysis
 mild sensory impairments
 transient paresthesias
 cardiac arrhythmias
 cranial nerve affectation (VII, IX, X)
 Extraocular mm & sphincters are rarely
affected
 Maintain respiratory function
 Prevent indirect impairments
 Prevent injury to denervated muscles
 Provide muscle reeducation
 Energy conservation techniques
 Cardiovascular fitness
 Provide emotional support
 Trauma
 Compression
 Vascular disorders
 Infection
 Tumors
 Metabolic disorders
 Vitamin deficiencies
 Toxicity
 Inflammatory diseases
Segmental demyelination

Axonal degeneration

Wallerian degeneration
Neuropraxia–a temporary interruption of
conduction without loss of axonal continuity
Axonotmesis–involves loss of the relative
continuity of the axon and its covering of
myelin, but preservation of epineuriumand
perineurium.
Neurotmesis–a total severance or disruption
of the entire nerve fiber.
First-Degree Injury (neuropraxia)
Second-Degree Injury (axonotmesis)
Third –Degree Injury – endoneurium
destruction
Fourth-Degree Injury – endoneurium
and perineurium destruction
Fifth-Degree Injury (neurotmesis)
Visual

Vestibular

Somatosensory
1.Stabilize visual images on the retina during
head movement for clear vision
2. Maintain postural stability during head
movements
3.Maintain spatial orientation
SEMICIRCULAR CANALS
 Horizontal SCC

 Posterior (inferior) SCC

 Anterior (superior) SCC

OTOLITH ORGANS
 Utricle

 Saccule
 SYMPTOMS PERIPHERAL CENTRAL
Balance deficits Mild ataxia Severe ataxia
Hearingloss With hearing loss no hearing loss

Nystagmus Jerk / Horizontal, resolve pendular/vertical

w/in 7 days nystagmus
Nausea Occasional with nausea
Additional Vertigo suppressed by visual severe vertigo cant be
neurologic fixation suppressed
impairment
Ocular tilt reaction (in
lesions above the
vestibular nuclei)
lateropulsion
can be a paroxysmal, single attack ofvertigo, a
series of attacks, or a persistent condition that
diminishes over three to six weeks
unilateral vestibular dysfunction and may be
associated withnausea,vomiting
PT Goals:
 combinations of head and eye movements, postural
changes, and walking exercises.
disorder of the inner ear
characterized by episodes ofvertigo, low-pitched
tinnitus, fluctuating hearing loss, and
sometimes a feeling of fullness or pressure in
your ear

PT Goals:
 stabilizing gaze, reducing dizziness and
increasing postural balance within the context
of activities of daily living
Drug ototoxicity (salicylates, aminoglycosides,
Quinine)
Infections: meningitis, encephalitis, Vestibular
neuritis
Otosclerosis-an abnormal bone growth in the
middle ear that causes hearing loss (idiopathic)
Nystagmus and vertigo with change in head
position, and occasionally nausea with or
without vomiting, and dysequilibrium.
 Cause: breaking off of otoconia

 Onset of vertigo/nystagmus: 15secs after

provocative positioning
 Duration: 60secs

 Test: Dix-HallpikeManeuver
Head-Shaking Induced Nystagmus
 Clinician flexes the head 30°before oscillating
horizontally for 20 cycles at a frequency of 2
reps/second (2 Hz)
 Observe for nystagmus