Anatomy

Lobes of the Brain

1. Frontal lobe is important for cognitive functions and control of voluntary movement or activity
2. Parietal lobe processes information about temperature, taste, touch and movement
3. Occipital lobe is primarily responsible for vision
4. Temporal lobe processes memories, integrating them with sensations of taste, sound, sight and touch.
Circle of Willis
The brain receives blood from two sources: the internal carotid arteries,
which arise at the point in the neck where the common carotid arteries bifurcate,
and the vertebral arteries. The internal carotid arteries branch to form two major
cerebral arteries, the anterior and middle cerebral arteries. The right and left
vertebral arteries come together at the level of the pons on the ventral surface of
the brainstem to form the midline basilar artery. The basilar artery joins the blood
supply from the internal carotids in an arterial ring at the base of the brain (in the
vicinity of the hypothalamus and cerebral peduncles) called the circle of Willis. The
posterior cerebral arteries arise at this confluence, as do two small bridging
arteries, the anterior and posterior communicating arteries. Conjoining the two
major sources of cerebral vascular supply via the circle of Willis presumably
improves the chances of any region of the brain continuing to receive blood if one
of the major arteries becomes occluded
The major branches that arise from the internal carotid artery—the
anterior and middle cerebral arteries—form the anterior circulation that supplies
the forebrain. These arteries also originate from the circle of Willis. Each gives rise
to branches that supply the cortex and branches that penetrate the basal surface
of the brain, supplying deep structures such as the basal ganglia, thalamus, and
internal capsule. Particularly prominent are the lenticulostriate arteries that branch
from the middle cerebral artery. These arteries supply the basal ganglia and
thalamus. The posterior circulation of the brain supplies the posterior cortex, the
midbrain, and the brainstem; it comprises arterial branches arising from the posterior cerebral, basilar, and vertebral arteries.
The pattern of arterial distribution is similar for all the subdivisions of the brainstem: Midline arteries supply medial structures,
lateral arteries supply the lateral brainstem, and dorsal-lateral arteries supply dorsal-lateral brainstem structures and the
cerebellum Among the most important dorsal-lateral arteries (also called long circumferential arteries) are the posterior
inferior cerebellar artery (PICA) and the anterior inferior cerebellar artery (AICA), which supply distinct regions of the medulla
and pons. These arteries, as well as branches of the basilar artery that penetrate the brainstem from its ventral and lateral
surfaces (called paramedian and short circumferential arteries), are especially common sites of occlusion and result in
specific functional deficits of cranial nerve, somatic sensory, and motor function
Brodmann’s Area Functions

1. Area 4 - precentral gyrus or primary motor area.

Functions:
a. Contralateral limb and face movements
b. Swallowing/laryngial movements
c. Volitional breathing control
d. Voluntary blinking
e. Horizontal saccadic eye movements
f. Contralateral thermal hyperalgesia

2. Area 6 - premotor or supplemental motor area.

Functions:
a. Motor sequencing/planning
b. Motor learning
c. Speech motor programming
d. Working memory
e. Movement initiation

3. Area 8 - facilitates eye movements and is involved in visual reflexes as well as pupil dilation and
constriction.

4. Areas 9, 10, and 11 - involved in cognitive processes like reasoning and judgment which may be
collectively called biological intelligence including executive function.

5. Areas 44 and 45- Broca's area; speech production.

6. Areas 3, 2, and 1 - somasthetic areas, meaning that they are the primary sensory areas for touch and
proprioception including kinesthesia.

7. Areas 5, 7, and 40 - presensory association areas where somatosensory processing occurs.

8. Area 39 is the angular gyrus. Functions include sentence generation, reading, calculation and visuospatial
processing.

9. Area 41 - Heschl's gyrus, the primary auditory area. It is the basic processing of auditory stimuli.

10. Area 42 -also involved in the detection and recognition of speech. The processing done in this area of
the cortex provides a more detailed analysis than that done in area 41.

11. Areas 21 and 22 - auditory association areas. Collectively they can be called Wernicke's area. It
selectively process text and speech.

12. Area 37 - Lesions here can cause anomia. Function includes semantic categorization and word retrieval.

13. Area 17 - the primary visual area. Specific functions include detection of light intensity and patterns,
visual attention and processing spatial orientation.

14. Areas 18 and 19 are the secondary visual (association) areas where visual processing occurs.

Motor and Sensory Homunculus

A cortical homunculus is a distorted representation of the human body, based on a neurological "map" of the
areas and proportions of the brain dedicated to processing motor functions, or sensory functions, for different
parts of the body.
PHYSIOLOGY
I. CNS Transmission of Impulses
This indicates that the first event in this sequence is a 'stimulus'.
'Stimuli' is the plural form, referring to more than one stimulus. In this context a stimulus is something that human
sensory receptors are able to detect, e.g. sounds, physical contact, tastes, visual sensation, etc..

The next stage in the pathway is the sensory receptors sensing the stimulus.
These receptors are located all over the body but some types of receptors are in specific areas of the body, e.g.
taste receptors in the mouth.

Sensory neuron(s) then transmit information from the sensory receptor(s) to the central nervous system (CNS),
i.e. the brain and spinal cord. This is happens because peripheral nerves connect to the spinal cord via the
network of nerves within the nervous system.

Information so received by the CNS is further transmitted by relay neurone(s) within the CNS. The information
may or may not be processed in the brain.

Some stimuli lead to 'reflex responses' that can be described in terms of the 'Simple Reflex Arc', whereas other
stimuli (such as all visual stimuli) always involve processing by the brain.

Following either simple reflex arc response, or processing by the brain, neural 'instructions' may be sent via a
motor neurone to an effector (usually a muscle or gland). In this way, the effector is instructed to take action. The
action may be physical movement of a muscle - hence perhaps also a body part such as a limb, or e.g. a
chemical action by a gland. Whatever the consequent action, this has occurred due to the function of the nervous
system, in response to the initial stimulus or stimuli.

II. CNS Neurotransmitters

1. Acetylcholine
- Found at neuromuscular junction
o Involved in muscle movements (nicotine, curare)
- In CNS: reticular activating system
o Slow excitation of cerebral neurons (muscarine, atrophine)
o Memory

2. Serotonin
- Involved in mood, depression
- Pain regulation
- Involved in regulation of cortical activity

3. Dopamine
- Involved in movement, attention, learning, motivation, reward

4. GABA (Gamma- Aminobutyric Acid)

- Main inhibitory neurotransmitter in CNS
- Also some anti-epileptic drugs
5. Norepinephrine
- also called noradrenaline, substance that is released predominantly from the ends of sympathetic nerve
fibres and that acts to increase the force of skeletal muscle contraction and the rate and force of contraction of
the heart. The actions of norepinephrine are vital to the fight-or-flight response, whereby the body prepares to
react to or retreat from an acute threat.

6. Endorphins
- any of a group of opiate proteins with pain-relieving properties that are found naturally in the brain. The
main substances identified as endorphins include the enkephalins, beta-endorphin, and dynorphin, which were
discovered in the 1970s by Roger Guillemin and other researchers. Endorphins are distributed in characteristic
patterns throughout the nervous system, with beta-endorphin found almost entirely in the pituitary gland.

7. Glutamate
- major excitatory transmitter in the brain

PATHOPHYSIOLOGY
· Ischemic Stroke
I. Cerebral Ischemia
Ischemic core vs Ischemic Penumbra

Ischemic Core – In the core area of stroke, blood flow is so drastically reduced that cells usually cannot recover
and subsequently undergo cellular death.

Ischemic Penumbra – It is the tissue in the region bordering the ischemic core. This region is rendered
functionally silent by reduced blood flow but remains metabolically active. Cells in this area are endangered but
not yet irreversibly damaged. They may undergo apoptosis after several hours or days but if blood flow and
oxygen delivery is restored shortly after the onset of stroke, they are potentially recoverable
II. Ischemic Cascade
i. Without adequate blood supply and thus lack of oxygen, brain cells lose their ability to produce energy -
particularly adenosine triphosphate (ATP).
ii. Cells in the affected area switch to anaerobic metabolism, which leads to a lesser production of ATP but
releases a by-product called lactic acid.
iii. Lactic acid is an irritant, which has the potential to destroy cells by disruption of the normal acid-base
balance in the brain.
iv. ATP-reliant ion transport pumps fail, causing the cell membrane to become depolarized; leading to a
large influx of ions, including calcium (Ca++), and an efflux of potassium.
v. Intracellular calcium levels become too high and trigger the release of the excitatory amino acid
neurotransmitter glutamate.
vi. Glutamate stimulates AMPA receptors and Ca++-permeable NMDA receptors, which leads to even
more calcium influx into cells.
vii. Excess calcium entry overexcites cells and activates proteases (enzymes which digest cell proteins),
lipases (enzymes which digest cell membranes) and free radicals formed as a result of the ischaemic cascade in
a process called excitotoxicity.
viii. As the cell's membrane is broken down by phospholipases, it becomes more permeable, and more
ions and harmful chemicals enter the cell.
ix. Mitochondria break down, releasing toxins and apoptotic factors into the cell.
x. Cells experience apoptosis.
 xi. If the cell dies through necrosis, it releases glutamate and toxic chemicals into the environment around
it. Toxins poison nearby neurons, and glutamate can overexcite them.
xii. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier and
contributes to cerebral oedema, which can cause secondary progression of the brain injury.
·
Hemorrhagic Stroke
Intracerebral vs Subarachnoid

1. Intracerebral haemorrhage – caused by rupture of a blood vessel and accumulation of blood within the
brain. This is commonly the result of blood vessel damage from chronic hypertension, vascular
malformations, or the use medications associated with increased bleeding rates, such as anticoagulants,
thrombolytics, and antiplatelet agents.

1. Subarachnoid haemorrhage is the gradual collection of blood in the subarachnoid space of the brain
dura, typically caused by trauma to the head or rupture of a cerebral aneurysm.

I. Rupture of a blood vessels

II. Compression of brain tissue from an expanding hematoma
III. Hematoma can distort and injure tissue. In addition, the pressure may lead to a loss of
blood supply to affected tissue with resulting infarction, and the blood released by brain hemorrhage appears to
have direct toxic effects on brain tissue and vasculature.

Embolic Stroke
Embolic Stroke may be due to multiple factors such as cardiac wall and chamber abnormalities, valve disorders
and arrhythmias.

Atrial Fibrillation – in AFib, the heart beats in an erratic way causing the inefficiency of each atrial contraction.
Blood not completely pumped out of the atria causes blood pooling. Blood pooling increases the risk of blood clot
formation. A blood clot formed in the atria can be dislodged and can circulate to the brain up to the small cerebral
vessels where it can get lodged thereby causing ischemia to the brain tissue.

Heart Failure –In HFs, the body tries to compensate to the inadequate oxygen supply by releasing hormones that
make blood more likely to clot. This may likely lead to embolic stroke.

Heart Valve Disease – Inefficient heart valves can cause regurgitation which can result in blood clot due to blood
stasis. Blood, cholesterol and other materials may stick and form small growths on the valves. These growths can
break off and ultimately travel to cerebral blood vessels where it can lodge into smaller vessels causing
decreased blood flow.

Heart Attacks – If heart attack injures one of the heart areas controlling the rhythm of the heart, it can cause
arrhythmia thus leading to increased risk of blood stasis ultimately leading to blood clot that can cause embolic
stroke.

ETIOLOGY
A. Modifiable Risk Factors for Stroke
1. Hypertension
· Most important risk factor
· Aggressive management of hypertension immediately after stroke should be avoided because of concerns
regarding maintaining flow distal to critical cerebrovascular stenosis
o Studies have shown that abrupt reductions in BP within 24 hours after stroke are associated with poorer
outcomes
2. Heart disease
· Hypertension and atherosclerosis
· Risk is doubled for those with CAD
· Atrial fibrillation and valvular heart disease increase the risk for cerebral infarction because both may cause
emboli
3. Smoking
4. Diabetes Mellitus
5. Elevated Fibrinogen
6. Erythrocytosis
7. Hyperlipidemia
8. Elevated homocysteine
· Associated with increased risk for ischemic stroke
· Can be lowered by supplementary vitamins but has not been found to reduce stroke risk
B. Non-modifiable Risk Factors
1. Age
2. Gender
3. Race
C. Risk Factors for Recurrent Stroke
· The probability of stroke recureence is highes early after a stroke
· For survivors of an initial stroke, the annual risk of a second stroke is approximately 5% but may be as high
as 42%
· Mortality after a stroke is high, with between 32% and 58% of initial survivors dead within 5 years after a
first stroke

EPIDEMIOLOGY
· 4th leading cause of death
· Leading cause of long term disability
· Men > Women but women over 85 yrs of age have increased risk than men
· African Americans > White Americans
· Increases dramatically with age (doubling after 65 yrs of age)
TYPES OF STROKE
Ischemic Hemorrhagic

Type Thrombotic Embolic Lacunar Intracerebral Subarachnoid

Hemorrhage

Risk Chronic HTN Atrial Fibrillation HTN Acute & chronic SACCULAR
Factors/ Atherosclerosi Mural Thrombus DM HTN ANEURYSM:
Associated s after MI, Cerebral congenital defect
conditions cardiomyopathy or amyloid in arterial wall
after cardiac angiopathy followed by
 surgery Use of progressive
Mechanical Heart anitcoagulants degeneration of
Valves Intracranial the adventitia
Septic Emboli tumor causing
Vasculitis ballooning of out-
pouching vessels
ARTERIOVENO
US
MALFORMATIO
N: congenital
structure
consisting of a
tangled web of
vascular tissue
that contains
multiple
arteriovenous
fistulas,
permitting arterial
to venous
shunting of blood

Pathophysio Large Cerebral emboli Microtatheroma Lipohyalinosis Rupture of

logy thrombus can (usually cardiac in Rapture of saccular
occlude major origin) lodge within Progressive microaneurysm aneurysm à
extracranial arterial branches of wall thickening s (Charcot- extravasation of
arteries major arteries &fibrinoid Bouchard blood à irritation
causing compromising necrosis aneurysm) of dura (can
ischemic injury blood flow distally cause headache)
to neural thereby inducing à sudden drop in
tissues ischemic injury to cerebral
supplied by neural tissue, glia & perfusion
the most distal vascular pressure (can
arterial endothelium cause loss of
branches consciousness)

Arteries Common MCA Ø Ø Small, deep SACCULAR

Involved & carotid Lenticulostriate penetrating ANEURYSM: MC
affected Vertebral arteries & small arteries in branches of
sites of the Arteries penetrating Ø Major lesions anterior
brain branches of occur in communicating
ACA, PCA & putamen and artery, ICA, &
Basilar artery thalamus, some MCA
Ø Subcortical in cerebellum
structures
including
internal
capsule, basal
ganglia,
thalamus &
brainstem

Presentation Ø Occurs MC Ø Sudden, focal LACUNAR Ø Severe HA & Ø Sudden

at night during neurologic SYNDROMES: major severe HA
 sleep or impairment Ø Pure motor neurological (described as
during periods Ø If cardioembolic, Ø Pure sensory deficits within worst headache
of inactivity onset of sx during Ø minutes of my life) with or
Ø Sudden activity or Sensorimotor Ø without focal
stuttering or associated ć Ø Dysarthria- Consciousness neurologic deficit
stepwise palpitations or clumsy hand becomes & often with
onset Valsalva maneuver Ø Ataxic progressively altered mental
Ø Pt. Hemiparesis impaired, ć status
awakens from Ø coma Ø Followed by
sleep ś deficits Hemiballismus developing vomiting & signs
Ø Pt.’s rapidly of meningeal
become aware Ø Results to irritation
of the deficits increase in ICP Ø Coma
when they frequently occurs
attempt to get Ø
out of the bed Hydrocephalus

Prognosis Ø Dependent Ø No cardiac Ø Earlier, more Ø Acute Ø SACCULAR

on the length thrombus after the rapid & greater mortality is high, ANEURYSM:
of time the event, only sudden degree of but those who within 6 months,
vessel is neurologic deficit neurologic survive often 50 % will rebleed
occluded, rate without previous or recovery experience Ø AVM: rate of
of flow through progressive compared to rapid neurologic bleeding is 6% in
the occluded symptoms other types recovery during the 1st year and
site, & the first 2-3 2-3% per year
effectiveness months after thereafter
of collateral hemorrhage
circulation
Ø Outcomes
may include
TIA’s, minor
stroke without
functional
compromise
or major
strokes
resulting to
significant
impairment &
functional
disability

SIGNS AND SYMPTOMS

1. Sudden numbness or weakness of face, arm, leg
2. Sudden confusion, trouble speaking or understanding speech
3. Sudden trouble seeing in one or both eyes
4. Sudden trouble walking, dizziness, loss of balance or coordination
5. Sudden severe headache with no known cause

COMPLICATIONS
Weakness and paralysis
- Weakness in the limbs is the most widely recognised effect of stroke. This weakness ranges in severity, with
some people only suffering from very mild weakness and others finding one whole side of their body is affected.
Paralysis may also occur, meaning a person loses the ability to move a body part altogether.

Spacticity
- Muscles may be left stiff, tight and painful to use after a stroke.

Difficulty walking
- A stroke sufferer may find their toes catch on the ground easily while they walk, a condition known of as
“drop foot.”

Changes in sensation
- A person’s sense of touch may be diminished, while sensitivity to pain may increase. Abnormal or
unpleasant sensations may also be experienced such as burning, tingling, stinging or numbness.

Memory
- Short term memory problems commonly arise and it can take longer for survivors to remember new
information.

Attention
- Survivors may find it hard to choose when they need to pay attention and when they don’t. Focusing on a
task may be difficult and it may become harder to concentrate, especially on several tasks at a time.

Depression
- Around 50% of stroke survivors develop depression after the event. Symptoms of depression vary in
severity and duration. Some of these symptoms include feeling sad, difficulty concentrating or making decisions,
loss of interest in daily activities and/or things that used to be of interest, anxiety, sleep disturbances, loss of
appetite, suicidal thoughts, self harming, loss of libido, loss of confidence and a tendency to avoid people.

Communication problems
- If stroke has caused damage to areas of the brain that are used in language, then communication may be
affected. This can also be affected if muscles in the face or throat have been damaged. Around one third of
survivors find their ability to communicate after a stroke is affected. The main conditions that cause
communication difficulties after a stroke are aphasia, dysarthria, and dyspraxia.

Aphasia
- Affects how a person speaks as well as their comprehension, reading and writing skills. Dysarthria causes
weakness in the muscles required to speak, which can change the sound of the voice and cause slurring.
Dyspraxia describes when the muscles fail to move in the order required to make the sounds needed for speech.

Emotional problems
- If the parts of the brain responsible for emotion are damaged by stroke then behavior, thought processes
and emotions may be altered. Survivors of stroke may experience emotions such as anger, anxiety, bewilderment
and frustration.

Fatigue
- Fatigue is a common after effect of stroke and survivors may lack energy, strength and feel constantly tired.
The fatigue experienced is unlike usual tiredness because it is not necessarily relieved by rest, nor is it related to
recent activity.

Visual problems
- Visual problems are also a common after effect of stroke, although they often resolve independently as the
brain starts to recover. In cases where the brain does not recover, these problems can be quite difficult to get
used to. The visual problems that arise depend on which brain parts are affected.

Decubitus Elcer
- There are four physical factors involved in the development of decubiti: pressure, shearing force, friction,
and moisture. The stroke patient is at increased risk of skin breakdown because of all four factors.
Additionally, stroke patients are often immobile, incontinent, and confused. Edema, sensory impairment,
malnutrition, poor circulation, and anemia also predispose to skin breakdown. It may also cause local
infection, pain, positioning problems, delay in amb.

Urinary tract infection

- The stroke patient is prone to developing a urinary tract infection because of many potential factors
including a preexistent atonic bladder, the change in urogenital flora with hospitalization, possible
comorbid conditions, such as malnutrition and prostate enlargement, poor perineal hygiene, and most
importandy, the common use of a Foley catheter.

Other complications
Constipation
Fecal impaction
Fecal incontinence
Urinary tract infection
Urinary retention
Urinary incontinence
Orthostatic hypotension
Deep venous thrombosis
Pulmonary embolism
Atelectasis
Aspiration pneumonia
Osteoporosis
Urinary tract stones
Deconditioning

PROGNOSIS
The patient prognosis after an ischemic stroke is much more positive than after a hemorrhagic stroke. In addition
to killing off brain cells, hemorrhagic stroke increases the risk of dangerous complications such as increased
intracranial pressure or spasms in the brain vasculature

MANAGEMENT
Medical Management
Medical management of completed stroke includes strategies to achieve the following:
Ø Improve cerebral perfusion by re-establishing circulation and oxygenation and assist in stopping progression
of the lesion to limit deficits. Oxygen is delivered via mask or nasal cannula. Patients in a coma may require
intubation or assisted ventilation and suctioning.
Ø Maintain adequate blood pressure. Hypotension or extreme hypertension is treated; antihypertension agents
have the added risk of inducing hypotension and decreasing cerebral perfusion.
Ø Maintain sufficient cardiac output. If the causes of stroke are cardiac in origin, medical management focuses
on control of arrhythmias and cardiac decompensation.
Ø Restore/maintain fluid and electrolyte balance.
Ø Maintain blood glucose levels within the normal range.
Ø Control seizures and infections.
Ø Control edema, intracranial pressure, and herniation using antiedema agents. Ventriculostomy may be
indicated to monitor and drain cerebrospinal fluid.
Ø Maintain bowel and bladder function, which may include urinary catheter. Catheterization is typically short-
term but may be long-term with the patient in coma.
Ø Maintain integrity of skin and joints by instituting protective positioning, a turning schedule every 2 hours, and
early physical and occupational therapy.
Ø Decrease the risk of complications such as DVT, aspiration, decubitus ulcers, and so forth.

Neurosurgical Management
Ø In hemorrhagic stroke, surgery may be indicated to repair a superficial ruptured aneurysm or AVM, prevent
rebleeding, and evacuate a clot (hematoma). Larger, deeper intracranial or brainstem vascular lesions are
generally not amenable to surgery. Surgery may also be indicated for resection of a superficial unruptured AVM
when there is high risk of rupture and stroke.
Ø Patients who are not eligible for tPA or who do not respond to tPA may be candidates for surgical intervention
using the Merci® Retriever System.
o This device is threaded via a catheter into a large artery just beyond the site of occlusion. It uses a tiny
corkscrew-shaped device that wraps around and traps the clot. The clot is then retrieved and slowly removed
from the artery. Blood flow is successfully restored.
o This system is not effective for smaller arteries and more distant locations.
Ø The Penumbra System® uses a catheter and separator that is threaded to the site of the clot. It suctions and
grabs the clot and aspirates the site.
o This system can be used effectively within an 8-hour window of symptom onset.
Ø Carotid endarterectomy is a surgical procedure used to remove fatty deposits from the carotid artery. It is a
useful procedure to prevent recurrent strokes or the development of stroke in individuals with TIAs. Stenosis of
60% to 99% is the typical guideline used when surgery is considered and can reduce stroke risk by as much as
55%. It cannot be performed with acute stroke because altered pressures could subject ischemic areas to further
damage.
Pharmacological Management
Ø Thrombolytics
Ø Anticoagulants
Ø Antiplatelet therapy
Ø Antihypertensive agents
Ø Angiotensin II receptor antagonist
Ø Anticholesterol agents/statins
Ø Antispasmodics/spasmolytics
Ø Antispastics
Ø Anticonvulsants
Ø Antidepressants
PT Management
A. Acute Phase
• Low intensity rehab is begun as soon as the patient is stabilized typically within 72 hours
• Early mobilization prevents or minimizes the harmful effects of bed rest and deconditioning and may also
increase patient’s level of consciousness
• Early stimulation and use of hemiparetic side
• Positioning, functional mobility training, ADL training and ROM
• Instructions and education to the patient and their family
B. Subacute Phase
C. Chronic Phase
• More than 6 months
• Interventions begun during the in-patient rehabilitation are continued and progressed
• Outpatient programs that target progressive improvements in flexibility, strength, balance, locomotion,
endurance and UE function have been found to be effective in producing meaningful outcomes
• Emphasize development of problem solving skills
• Fall risk factors should be eliminated or minimized
PT Interventions
A. Improve Motor Learning
a. Strategy Development
b. Feedback
c. Practice
B. Improve Sensory Function
a. Sensory Retraining Program
• Mirror therapy, repetitive sensory discrimantion activities, bilateral simultaneous movement and repetitive
task practice
b. Sensory Stimulation Intervention
• Compression techniques, mobilization, electrical stimulation, thermal stimulation or magnetic stimulation
C. Improve Flexibility and Joint Integrity
D. Improve Strength
E. Improve Movement Control
F. Improve Functional Status
a. Bed Mobility
b. Sitting
c. Transfers
d. Standing
G. Improve Postural Control and Balance
H. Improve Gait and Locomotion
a. Task specific Overground locomotor training
b. FES
c. Orthotics and Assistive devices
d. Wheelchairs
I. Improve Aerobic Capacity and Endurance
· During post-acute stage, use of cycle ergometer and treadmill
· Patients with balance impairment would benefit more from treadmill training
· Circuit class training

DIFFERENTIAL DIAGNOSIS
1. Internal Carotid Artery
· Massive cerebral infarction in the distribution of the ACA and MCA with rapid severe obtundation, with
head and eyes turned toward the side of the lesion
· Often cerebral edema with transtentorial herniation and death
· Anterior cerebral circulation may be preserved through flow from the opposite side via the anterior
communicating artery
· First branch of the ICA is the ophthalmic (retinal branch)
- transient occlusion produces sudden, loss of vision in one eye
- If inadequate collateral flow through the orbit from the ECA à ipsilateral blindness from retinal ischemia
on the side of the lesion associated with contralateral hemiplegia.
o Dense contralateral motor and sensory deficits
2. Anterior Cerebral Artery
· Clinical manifestations
Signs and Symptoms Structures Involved

Contralateral hemiparesis involving mainly the Primary motor area, medial aspect of cortex,
LE (UE is more spared) internal capsule

Contralateral hemisensory loss involving Primary sensory area, medial aspect of cortex
mainly the LE (UE is more spared)

Urinary Incontinence Posteromedial aspect of superior frontal gyrus

Problems with imitation and bimanual tasks, Corpus callosum

apraxia

Abulia (akinetic mutism), slowness, delay, lack Uncertain localization

of spontaneity, motor inaction

Contralateral grasp reflex, sucking reflex Uncertain localization

Can be asymptomatic if circle of Willis is
competent

3. Posterior Cerebral Artery

Signs and Symptoms Structures involved

Peripheral territory

Contralateral homonymous hemianopsia Primary visual cortex or optic radiation

Bilateral homonymous hemianopsia with some Calcarine cortex (macular sparing is due to
degree of macular sparing occipital pole receiving collateral blood supply
from MCA)

Visual agnosia Left occipital lobe

Prosopagnosia (difficulty naming people on Visual association cortex

sight)

Dyslexia (difficulty reading) without agraphia Dominant calcarine lesion and posterior part of
9difficulty writing), color naming (anomia), and corpus callosum
color discrimination problems
 Memory defect Lesion of inferomedial portions of temporal lobe
bilaterally or on the dominant side only

Topographic disorientation Nondominant primary visual area, usually

bilaterally

Central Territory

Central post-stroke (thalamic) pain Ventral posterolateral nucleus of thalamus

Spontaneous pain and dysesthesias; sensory
impairments (all modalities)

Involuntary movements; choreoathetosis, Subthalamic nucleus or its pallidal connections

intention tremor, hemiballismus

Contralateral hemiplegia Cerebral peduncle of midbrain

Weber’s syndrome Third nerve and cerebral peduncle of midbrain

Oculomotor nerve palsy and contralateral
hemiplegia

Paresis of vertical eye movements, slight miosis Supranuclear fibers to third cranial nerve
and ptosis, and sluggish pupillary light response

Gen Info
Pt’s name: A.B.
Age: 65 y.o
Sex: F
Address: Antipolo City
Civil Status: Married
Handedness: R
Occupation: Retired Teacher
Rehab MD: Dr. C.D.
Date of Rehab/Consult: December 6,2017
Date of IE: December 11, 2017
MD Dx: L MCA Infarct

HPI>
Present condition started ~6 months Pt was diagnosed c L Thrombotic MCA infarct. Pt was then confined for 2
weeks and received in-patient physical therapy where she was given ROM exercises, taught DDBE, GBRE and
proper positioning. Upon d/c pt stayed at home to rest and was asked to return to hospital for check up p 2
weeks.

5 mos. PTIE, Pt was referred to PT rehabilitation by her Neuro MD as an out-patient. PTMx include ROM
exercises, stretching exercises and sitting and standing tolerance exercises and ambulation inside // bars. Pt
attended her rehab sessions for 3 mos, but, d/t the busy schedule of her daughter, which is her primary caregiver,
they decided to continue therapy through home exercise program. 2 mos prior to PTIE, Pt proceeded c her
exercises but c irregular schedule as pt became lazy and started to lose interest in doing the exercises. Pt’s
daughter was also busy to supervise her mother’s exercises. As a result, pt's activities at home only include
sitting, watching TV or lying on the bed most of the time. Pt then became dependent on her daughter when
performing ADLs such as bathing, dressing, transfers and bed mobility. Pt reported that she was still able to
ambulate but presents c circumducting gait and requires +1 mod assist

3 weeks PTIE, pt's daughter noticed that the pt's condition was becoming worse as pt presents c difficulty upon
ambulation and upon performing R UE movements or as described by the pt’s daughter, "parang nanigas yung
kamay niya". Pt’s daughter also noticed that pt cannot perform any activity s assistance as pt tends to lose her
balance. This prompted pt's daughter to have her mother checked by a rehab doctor again.

1 week PTIE, pt was again referred to PT rehab as an out pt to continue her PT rehab sessions and for further
assessment and management.

PMHX
(+) Controlled Htn (since 2010)
(+) Controlled Hypercholesterolemia (since 2010)
(-) CA
(-) RA
(-) Dizziness episodes
(-) TIA
(-) Vestibular Syndromes
(-) DM
(-) Cardiovascular Disease
(-) Pulmonary Disease
(-) Allergy
(-) Trauma

FMHx

MOTHER FATHER

Cardiac disease (-) (+)

HTN (-) (+)

Stroke (-) (+)

DM (-) (-)

Pulmo Disease (-) (-)

CA (-) (-)

Hypercholesterolemia (-) (-)

PSHx:

 Pt is a non-cigarette smoker and non-alcoholic beverage drinker

 Pt has a sedentary lifestyle and usually stays at home watching TV
 During her pre morbid status, pt would sometimes cook for her family, attends mass q Sunday and goes
to the mall c her family. Pt also walks around their village for ~30 mins, 2x/wk
 Pt's diet includes meat, rice and little fruits and vegetables
 Pt does not use prohibited drugs

Home Situation:
Pt lives c her husband and daughter (25 y.o.). Pt's daughter will be her primary caregiver. Pt lives c a helper that
will also assist her and help them c household chores. Pt's pension will be the main source of her rehab
expenses.

Environmental Assessment:
· Home:
Pt lives in a bungalow type house. All areas are well lit c non skid type of flooring. Using the main door as the
reference, the ff measurements were obtained: pt’ room is at the 2nd floor with 20 steps of stairs.
Living room ~2m
Kitchen ~4m
Dining room ~3m
Bathroom ~5m
Pt's Bedroom ~5m
Ht of bed: ~ 0.75 m
Ht of chair: ~ 0.50 m
Using the floor as reference, the following height measurements are taken:
● Cabinet: ~ 1.5 m
● Window: ~ 1 m
● Light switches: ~1.5m
● Door knobs: ~1 m
● Sink: ~1.2 m
● Study table: ~ 1 m
● Clothesline: ~1.6 m
● TV: ~1. 3 m c screen on eye-levelled height

Village
 Pt walks around the village on level surfaces ~200 m

Mode of transportation
 Pt rides a car driven by her husband going to church and mall

Ancillary Procedures:
Date Performed Results
 CT Scan (Sagittal Coronal) July 11, 2017 (+) Infarct on L
Frontotemporoparietal lobe

Meds Taken

Drug Dosage/Frequency Indication Last taken

Aspirin 80 mg/od Anticoagulants December 11, 2017

Amlodipine 10 mg/od HTN December 11, 2017

Rosuvastatin 20 mg/od Hypercholesterolemia December 11, 2017

S>
C/C: Pt ℅ stiffness on R UE and feeling of losing balance resulting to difficulty in self care activities, transfer and
ambulation
Pt’s goal: Pt wants to ambulate independently s losing balance

O:
VS
Before After

BP 110/80 mmHg 120/80 mmHg

HR 72 bpm 75 bpm

RR 15 cpm 17 cpm

Temp 36.8 deg C 36.6 deg C

O2 sat 99 % 99 %
Findings: All VS are WNL.
Significance: For baseline purposes. Pt may proceed to rehab session safely

OI
Wheelchair borne
Alert, coherent, cooperative
Ectomorph
(+) Typical arm posture on R UE
(+) Postural deviation (see PA)
(+) Gait deviation (see Gait A)
(+) Muscle atrophy on R shoulder
(-) Slurring speech
(-) Facial asymmetry
(-) Sialorrhea
(-) arm sling
(-) Orthosis on R UE and LE
(-) Swelling on R UE/LE
(-) Redness on B UE/LE
(-) Gross Deformities on B UE/LE
(-) Trophic skin changes on R UE/LE

Palpation
Normothermic on all exposed areas
(+) Hypertonic on R UE/LE (see Tone A)
(+) ~1 fingerbreadth R shoulder subluxation
(+) mm guarding towards all motions of R UE and LE
(-) Edema on B UE/LE
(-) Crepitation on B UE/LE
(-) Tenderness on B UE/LE
(-) Ms spasm on B UE/LE

ROM
All major joints of (B) UE/LE and trunk were actively & passively assessed & found to be WNL, painfree c N end
feel except:
Motion AROM PROM Normal DIFFERENCE END-FEEL

R shoulder flexion 0-40 0-140 0-180 140/40 Empty

R shoulder ext 0-20 0-40 0-60 40/20 Empty

R shoulder abd 0-40 0-120 0-180 140/60 Empty

R elbow flexion 0-110 0-150 0-150 40/0 Empty

R elbow ext 110-80 150-0 150-0 80/0 Empty

R wrist flex 0-70 0-70 0-80 10/10 Firm

R wrist ext 0-40 0-70 0-70 30/0 Empty

R hip flexion 0-50 0-90 0-120 40/30 Firm

R hip abduction 0-20 0-30 0-45 25/15 Firm

R hip IR 0-10 0-20 0-45 35/25 Firm

R hip ER 0-15 0-30 0-45 30/15 Firm

R knee flexion 0-100 0-135 0-135 35/0 Soft

 R knee ext 100-0 100-0 135-0 35/0 Hard

R ankle DF 0-10 0-20 0-20 20/0 Firm

R ankle PF 0-20 0-40 0-50 30/10 Firm

Findings: (+) LOM on (R) UE & LE in 2˚ to weakness, pain and tightness

Significance: Pt will have difficulty in performing ADLs such as self-care, transfers, bed mobility and amb.

FMT
Pt was assessed in sitting position
Task Grade
R L
Hand to top of the head. WF F
Hand to mouth. F F
Hand to opposite ear. WF F
Hand to opposite shoulder. WF F
Hand to umbilicus WF F
Hand to back WF F
Heel to opposite toe. F F
Heel to opposite shin. F F
Heel to opposite knee. WF F

Legend:
Functional (F) Normal/able to perform
Weak Functional (WF) Moderate Impairment/Able to perform but sluggishly c limitation d/t weakness
Non-Functional (NF) Severe Impairment/ not able to perform
Findings: Pt has weakness on muscles of R UE. This can be associated c presence of spasticity
Significance: Pt will have difficulty doing overhead activities

MMT
All major muscle groups of L UE and B LE are graded 5/5 assessed using standard MMT except:
Muscle group Grade
R hip flexor 4/5
R hip extensor 3/5
R hip abductor 4/5
R ankle dorsiflexor 4/5
Findings: Pt has weakness on R LE due to disuse and spasticty
Significance: Pt may have difficulty in performing bed mobility, transfers and ambulation

Neurologic A:
Superficial sensation

Spf. Modality used Area tested % of intact sensation

Sensation
 R L

Light touch Brush Face 70 % 100 %

Upper arm 70 % 100%

Forearm 70 % 100%

Thigh 70 % 100%

Lower leg 70 % 100%

Foot 70 % 100%

Pain Pointed end of Face 70 % 100%

neurohammer
Upper arm 70 % 100%

Forearm 70 % 100%

Thigh 70 % 100%

Lower leg 70 % 100%

Foot 70 % 100%

Pressure PT's thumb Face 70 % 100%

Upper arm 70 % 100%

Forearm 70 % 100%

Thigh 70 % 100%

Lower leg 70 % 100%

Foot 70 % 100%

Findings: Pt has sensory deficits on R UE and LE

Significance: (+) affectation of BA 3,1,2 and for precautionary purposes when using modalities.

Deep sensation

Test Procedure R L
 Proprioception Moving each DIP jt up & down. Pt is 4/5 Able to determine
then asked where the end position of end position of B UE
the extremity is. Tested on B (5/5) & LE (5/5)
extremities.

Kinesthesia Moving each DIP jt up and down. Pt 3/5 Difficulty in

is then asked in what direction the determining direction
digit is moving. Tested on B of mov't on B UE (5/5)
extremities. & LE (5/5)
Findings: Pt. has deficits on proprioception and kinesthesia on R UE/LE.
Significance: This may affect Pt’s balance during ambulation

Cortical sensation:

Test Stimulus R L

Stereognosis Key, watch, coin 3/3 3/3

Graphesthesia S, O, M, L, J 4/5 5/5

Findings: Pt has minimal deficits on cortical sensation on R UE.

Significance: To check extent of affectation

Tone A:
All major mm groups of B UE and LE are normotonic except:
Using Modified Ashworth scale:
Muscle Grade

R shoulder adductor 1+

R elbow flexor 2

R wrist flexor 1+

R hip adductor 1+

R knee extensor 1

R ankle plantarflexor 1+

Legend: Modified Ashworth Scale

0 No increase in ms tone

1 Slight increase in ms tone, manifested by a catch & release or by minimal resistance at the end
of the ROM when the affected part(s) is moved in flexion or extension
1+ Slight increase in ms tone, manifested by catch, followed by minimal resistance throughout the
remainder (less than half of the ROM)

2 More marked increase in ms tone through most of the ROM, but affected part(s) easily moved

3 Considerable increase in ms tone, passive movement difficulty

4 Affected part(s) is rigid in flexion/extension

Findings: Pt has spasticity on R UE and LE

Significance: Pt will have difficulty in performing ADLs such as self care, bed mobility, and amb.

CN Testing

CN Stimulus Results/Findings

1 Coffee Intact: Pt was able to identify

2 Pupillary light Intact: B eyes constricted

3, 4, 6 Lateral, medial, downward and upward Pt was able to follow examiner’s finger in all directions on B
movements of eyeball eyes.

5 Facial sensation Intact spf sensation (See sensory test)

Corneal Reflex (+) Blinking on B eyes upon wisp of cotton
Open & clench teeth Pt was able to perform opening & clenching of teeth.

7 Facial mm expression as to opening Intact: Pt was to perform facial mm expression s difficulty.

eyes & closing eyes forcefully, wrinkle
forehead, frowning, pouting, puffing
cheeks & smiling.

8 Rubbing hair strands ~2in from ear. Intact: Pt was able to localize
Tested on B

9, 10 Swallowing Intact: Pt was able to swallow s difficulty

11 Shoulder shrug, SCM action Pt was able to perform B shoulder shrugs and SCM actions

12 Move tongue rapidly in Intact: Pt was able to perform. (-) Tongue atrophy
side to side direction

Findings: All CN are intact.

Significance: To check for brainstem affectation and extent of injury.

DTR
 R L

+++ ++
+++ ++

++ + ++

+++ ++

Findings: (+) UMNL. Normoreflexive on L UE/LE but is hyperreflexive on ® UE/LE.

Significance: To check extent of injury.

Pathologic Reflex
R L

Babinski sign (-) (-)

Clonus (-) (-)

Hoffmann’s (-) (-)

Findings: Pt has absent pathologic reflex on B UE and LE

Significance: Pt may perform ambulation safely

Anthropometric Measurement

Muscle Bulk Measurement

Landmark R L Difference

10 cm from acromion 28 cm 30.5 cm 2.5 cm

process

10 cm from lateral 22 cm 25.5 cm 3.5 cm

epicondyle of humerus

15 cm from ASIS 31 cm 34 cm 3 cm

10 cm from tibial 30 cm 32 cm 2 cm
tuberosity
Findings: Pt showed significant difference in the muscle bulk measurement of B UE and LE
Significance: Pt does presents c atrophy on R UE and LE due to disuse

Postural A:
All major bony landmarks are within N alignment assessed in unsupported standing position except:
 Anterior Posterior Lateral

R shoulder adducted and R scapula protracted Ear anterior to acromion

internally rotated

R elbow flexed Decreased cervical lordosis

R wrist flexed Increased thoracic kyphosis

R fingers flexed Decreased lumbar lordosis

Findings: Pt presents with typical arm posture
Significance: Pt will have difficulty performing reaching activities. Pt may also have increased risk of fall

Gait A:
Pt was assessed in independent ambulation s AD
Stance Phase
 Decreased R hip flexion, knee extension and ankle dorsiflexion during initial contact
 Decreased R hip and knee extension during midstance
 Decreased R hip extension during terminal stance
Swing Phase
 Decreased R hip and knee flexion during initial to midswing
 Decreased R hip and knee flexion and ankle dorsiflexion during late swing
Gait Parameters
Step length ↓
Stride length ↓
Step width ↓
Walking speed ↓
Cadence ↓
Arm swing ↓
Trunk rotation ↓

Findings: Pt presents c circumducting gait

Significance: Pt may have difficulty in ambulation due to increased energy expenditure and risk of fall

CardioPulmo A:
Cardiac A:
 Auscultation: Normal rhythm, (-) murmurs

Pulmo A:
 Inspection
 N breathing pattern
 (-) cyanosis
 (-) labored breathing
 (-) use of accessory muscles of respiration
 Palpation
 N tactile fremitus on all areas
 Chest Expansion Measurement

Landmark Inhalation Exhalation Difference

 Axilla 79 cm 76 cm 3 cm
T4 78 cm 75 cm 3 cm
Xiphoid process 75.5 cm 72 cm 3.5 cm

 Auscultation
 Normal rhythm
 (-) abnormal breath sounds

Findings: Pt has normal cardiopulmonary system as to inspection, palpation and auscultation. Pt does not show
any signs of abnormality. However, Pt has decreased chest expansion on axillary area.
Significance: Pt has minimal decreased in chest expansion. This might affect Pt’s endurance during ambulation

Endurance Testing:
Pt was assessed in independent level ambulation c rolling walker using 6 minute walk test
Time Distance covered Rest RPE BP (mmHg)
0 – 1 min and 40 s 40 m 0 13 120/80
1 min 40 s – 3 min 5 0 m 1 (1 min 25 s) 11 130/80
s
3 mins 5 s – 6 min 50 m 0 11 130/80
Total: 90 m
Findings: Pt has decreased endurance as manifested by decreased distance covered and presence of rest
period. This might be associated c Pt’s deconditioning and previous pulmonary condition
Significance: Pt may have difficulty performing ambulation for prolonged period of time

Functional A:
Pt was assessed in independent standing position inside // bars
Sitting Standing

Balance Normal Good

Tolerance Normal Fair

Findings: Pt presents c decreased standing balance and tolerance
Significance: Pt may have difficulty maintaining standing position for prolonged period. Proper guarding should
also be observed during ambulation
ADL A:

Activity Performance

Feeding Pt feeds in modified

independence. Pt feeds in
short sitting position using L
UE for reaching food as well
as for holding the spoon. Pt’s
R UE remains at her lap

Bathing Pt bathes in modified

independence. Pt bathes in
sitting position using L UE
 only with slowness in
movement. Pt’s R UE
remains at her side

Grooming Pt performs grooming

independently. Pt uses her L
UE in combing and brushing
while R UE remains at her
side

Toileting Pt performs toileting in

modified independence. Pt
uses her L UE in washing
buttocks but in a slow
manner.

Dressing Pt needs +1 moderate assist

in dressing B UE and LE. Pt
asks her caregiver to don
and doff her clothes due to
inability to elevate shoulders
efficiently

Supine to side-lying Pt moves from supine to

side-lying independently. Pt
reaches the opposite side of
bed using L UE while
pushing on the bed using L
foot c knee slightly flexed to
initiate and complete the
activity

Side-lying to short sitting Pt needs +1 minimal assist in

moving into sitting position.
Pt was able to do lateral
cervical and trunk flexion in
minimal range. Pt tries to
push on bed using her L UE,
however it is insufficient in
order for the Pt to lift her
body off the bed resulting to
the need of assistance on
shoulder and pelvis

STS Pt moves from sitting to

standing in modified
independence. Pt pushes the
 surface of bed using R hand
to help propel the body
upward.

Level ambulation Pt ambulates c +1 minimal

assist but with gait deviation
and slowness in movement
due to feeling of losing
balance

Findings: Pt performs most of ADLs in modified independence

Significance: Pt has modifications in almost all activities due to weakness and tightness on L UE and LE

A:
PT Diagnosis
MDDx of L MCA Infarct futher defined by LOM, weakness, atrophy, spasticity, postural deviation, gait deviation,
good standing balance and fair standing tolerance resulting to difficulty in performing ambulation and ADLs

PT Impression
PT Prognosis
Pt has a good prognosis as to independent level ambulation c quadcane since Pt was given immediate medical
intervention and Pt received in-patient and out-patient PT. Pt also has preserve strength of L UE and B LE. Pt
has no other comorbidities except for Htn and Hypercholesterolemia which is controlled by medication and
lifestyle modifications. Limitation in ROM as well as muscle strength can be improved by exercises. However, Pt’s
condition is in Brunnstrom stage 3, chronic stage and marked spasticity is still present which could hinder the Pt
from performing the activity. Secondary complications such as pressure sore, contracture and further atrophy can
be prevented by home exercises and Pt education.
Rehab Potential: Pt has good rehab potential because pt is motivated to undergo rehab and is willing to do all the
PTMx. Pt’s family is supportive and is financially stable.

Problem list
1. Difficulty in level ambulation
2. Good standing balance
3. LOM towards all motions of R UE and LE
4. Weakness on R hip flexor, abductor and ankle dorsiflexor
5. Gait deviation
6. Decreased endurance
7. Fair standing tolerance
8. Postural deviation
9. Difficulty in self-care activities
10. Atrophy on R UE and LE
11. Sensory deficits on R UE and LE
12. Spasticity on R UE and LE
LTG
Pt will continuously ambulate independently c quadcane using 3 point gait on level surfaces around the
village ~200 m s risk of fall p 6 wks

STG
1. Pt will have increased ROM on all motions of R UE and LE c a total of 10 degree increment in 2 wks
2. Pt will present proper postural alignment c normal cervical lordosis and thoracic kyphosis in 2 wks
3. Pt will have good standing tolerance in 3 wks
4. Pt will have normal standing balance in 3 wks
5. Pt will continuously ambulate independently c quadcane using 3 point gait on level surfaces ~100 m s
risk of fall in 3 wks
6. Pt will have increased endurance as manifested by increased distance walked in 6MWT by ~50 m c
RPE of 11 in 4 wks
7. Pt will have normal strength on R hip flexor, abductor and ankle dorsiflexor in 6 wks
8. Pt will maintain skin, muscle and joint integrity as manifested by absence of pressure sore, contracture
and further atrophy in 6 wks

P:
Pt will be seen for 3x/week for 6 wks
1. DDBE x 4 rep q waking hr to promote effective breathing
2. AAROMEs of ® UE on AP in sitting x 10 reps x 1 set to maintain joint mobility

2. AROME of (L) UE and B LE on AP in sitting x 10 reps x 1 set to maintain joint mobility

3. AROME of face in sitting x 10 reps x 1 set to maintain joint mobility
4. Stretching towards R shoulder flexion and abduction, wrist extension, hip flexion and abduction and ankle
dorsiflexion x 30 SH x 3 reps x 1 set to increase ROM
5. LE ergo x 15 mins to increase endurance
6. Bed mobility ex to improve independent function on bed
I. Side-lying to short sitting towards R side
Part Practice
a. Active lateral cervical flexion towards R x 5 reps x 1 set
b. Pushing of R hand against bed x 5 reps x 1 set
Whole Practice
c. Side-lying to sitting towards R side x 3 reps x 1 set
7. Transfer from bed ↔ chair exercise to improve manner of transfer:
Part practice
 Scooting forward x 5 reps x 1 set
Whole practice
 Transfer from bed ↔ chair by stepping of feet x 3 reps x 1 set
8. STS ex in // bars to improve pt’s transition from sitting to standing
Part Practice
• Scooting forward x 10 reps x 1 set
• Backward foot placement x 5 reps x 1 set
• Forward trunk movement at hips x 10 reps x 1 set
• Knee flexion x 10 reps x 1 set
Whole Practice
• Sit to stand x 3 reps x 1 set

9. Standing balance exercises observing proper postural alignment

a. Lateral weight shifting incorporating heavy joint compression of ® hip x 10 reps x 1 set
b. Forward-backward weight shifting x 10 reps x 1 set
 c. Cone reaching x 10 reps x 1 set
10. Gait training on level surfaces inside parallel bars to improve quality of gait
Part Practice
 Stepping exercise emphasizing R hip flexion and weight bearing on L LE x 10 reps x 1 set
 ROM of B knee flexion and extension x 10 reps x 1 set in sitting
 Toe raises x 10 reps x 1 set
 Side ward walking x 10 reps x 1 set
Whole Practice
 Ambulation inside parallel bars c quadcane using 3 point gait x 3 rounds
 Ambulation clearing cones x 3 rounds

Progression:
1. PREs of L UE and B LE using 2 lbs DB & 2 lbs AW x 10 reps x 1 set to improve strength
2. LE ergo x 20 mins to improve endurance
3. Gait training on level surfaces outside parallel bars as tolerated to improve
quality of gait
Part Practice
 Stepping on foot stool emphasizing R hip flexion x 10 reps
Whole practice
 Ambulation outside parallel bars c quadcane using 3 point gait pattern x 3 rounds
 Ambulation clearing cones x 3 rounds

HEP
1. AAROME of ® UE on AP x 10 res x 1 set
2. AROME of (L) UE and B LE on AP x 10 reps x 1 set
3. DDBE x 4 reps q waking hour
4. Household amb x as tolerated emphasizing R hip and knee flexion and ankle dorsiflexion during initial
contact and mid to terminal swing

Pt Education
1. Check skin of Pt regularly especially on the sacrum, ischial tuberosity and malleoli.
2. Change the position of Pt on bed every 2 hours and on chair every 30 mins to prevent secondary
complications
3. Remind Pt regarding proper postural alignment emphasizing head and trunk in midline using verbal,
tactile and proprioceptive cues
4. Observe rest periods in between exercises to prevent over exertion