1
Q
Neurological condition which causes the unilateral paralysis of the face.
A
BELL’S PALSY
2
Q
is both motor and sensory, and it arises from the brainstem in between the pons and medulla. The facial nerve is also subdivided in to 5 branches.
A
CN VII (Facial nerve)-
3
Q
There are five branches of the facial nerve which are responsible for the movement and sensation of the face, these five are:
A
- Temporal Branch- innervates the frontalis, orbicularis oculi and corrugator supercilli.
- Zygomatic Branch- innervates some parts of the orbicularis oculi.
- Buccal Branch- innervates the orbicularis oris, buccinators and zygomaticus muscle
- Marginal Mandibular Branch- innervates the mentalis, depressor labii inferioris and depressor anguli oris.
- Cervical Branch-innervates platysma muscle.
4
Q
Name and Location of Primary Nuclei:
A
- Facial Motor Nucleus- Responsible for the muscles of facial expression.
- Superior Salivatory Nucleus- responsible for the salivary and lacrimal glands.
- Nucleus of Spinal Tract- responsible for the sensory at external ear and tympanic membrane.
- Nucleus Solitarius- Responsible for the sense of taste.
5
Q
Movements of the muscles innervated by the facial nerve:
A
-Frontalis- wrinkling of the forehead and raising of eyebrows.
-Orbicularis Oculi – closing of the eyes.
-Corrugator Supercilli- frowning and vertical wrinkling of forehead.
-Orbicularis Oris- kissing pose of the lips and closing of the mouth.
-Buccinator- puffing the cheeks.
-Risorius- Smiling without the teeth showing.
-Nasalis- “flaring”/ enlarging of the nostrils.
-Mentalis- allows the lips to “pout” and chin to wrinkle.
-Zygomaticus- Elevates both corners of the mouth when smiling, shows teeth.
Platysma- Depresses both angles of the mouth.
6
Q
Epidemiology of Bells Palsy
A
- More present in males than of the females
- Peeks from ages 20 to 40 years of age.
- Diabetic patients are most likely to develop this condition, up to four times more.
- Pregnant women are also susceptible of this condition.
- Most common acute condition which has only one nerve involved.
7
Q
Etiology of Bells palsy
A
- Hereditary
- Swelling or inflammation of the nerve involved.
- Exposure to viral infections such as:
- Herpes Simplex
-Herpes Zoster
-Rubella
-Mumps Virus
-Cold Flue
-HFMD - Diabetes
- Acute respiratory tract infection
- Tumor which invade the temporal bone
- Fracture of the temporal bone
- Lymphocytes- mediated hypersensitivity phenomenon
- Middle ear infection
- Meningitis
8
Q
TYPES/CLASSIFICATION (bells palsy)
A
- Unilateral noncurrent
- Unilateral recurrent
- Simultaneous bilateral
- Alternating bilateral
- Recurrent bilateral type
9
Q
CLINICAL MANIFESTATION (bells palsy)
Signs and symptoms depend upon the location of lesions as follows:
Lesion1: Outside the stylomastoid Foramen
A
Widened palpebral fissure due to paralysis of the orbicularis palpebrum
The forehead cannot wrinkle *
The upper eyelid closes slowly *
In a complete facial paralysis, when attempt to shut the eye, closure is incomplete and the eyeball rolls upward and outward, demonstrating Bell’s phenomenon
Blinking reflex is loss on the affected side *
Saliva may dribble on the mouth
There is no deviation of the tongue or jaw
10
Q
Lesion 2: In facial canal involving the chorda tympani *
A
Loss of taste in the anterior 2/3 of the tongue
Reduced salivation on the affected side
11
Q
Lesion 3: Higher in the facial canal involving the stapedius muscle
A
All sign of lesion 1 and 2
Hyperacusis- painful sensitivity to loud sound
12
Q
Lesion 4: Higher involving the geniculate ganglion *
A
All signs of 1-3 *
Pain behind and within the ear
13
Q
Lesion 5: In the internal auditory meatus
A
Signs of Bell’s Palsy *
Deafness (CN8)
*Tinnitus
14
Q
Lesion 6: at the emerges of facial nerve from pons *
A
Involvement of CN 5 and 8 *
May also involve CN 6,11 and 12
Marcus-Gunn or Jaw winking phenomenon-elevation of ptotic eyelid on movement of jaw to the contralateral side. *
Marin Amat Syndrome- closing of eyelids during mouth opening
15
Q
Phenomenon seen in Bell’s Palsy
A
- Marcus Gunn Phenomenon- elevation of ptotic eyelids during movement of the jaw
- Marin- Amat Syndrome- opening of the mouth causes eye closure
- Moebius Syndrome- bilateral facial paralysis
16
Q
Sign and Symptoms of Bells palsy
A
Acute onset unilateral upper and lower facial paralysis (over a 48-hr period)
Posterior auricular pain
Hyperacusis
Taste disturbances
Otalgia
Weakness of the facial mm.
Poor eyelid closure
Aching of the ear or mastoid
Tingling or numbness of the check/mouth
Epiphora - excessive watering of eyes
Ocular Pain
Blurred vision
Flattening of forehead and nasolabial fold on the side affected by palsy
17
Q
Complication that may appear after apparent recovery: BP
A
State of over toning or contracture
Associated movement of synkenesis
18
Q
- unilateral lacrimation on eating on due to regeneration facial nerve fibers
- hemifacial Spasm- spasm of facial muscle usually begins in orbicularis oculi
A
Crocodile Tears (aka Bogorads Syndrome, Gustatoclarimal reflex, Paroxysmal lacrimation)BP
19
Q
confirms the presence of nerve damage and determines the severity. An _____ measure the electrical activity of a muscle in response to stimulation and the nature and speed of the conduction
A
DIAGNOSIS
: Laboratory Test Electromyography- BP
20
Q
Dx: Imaging scan:BP
A
X-ray Imaging, MRI or CT scan may be needed on occasion to rule out other possible sources of pressure of the facial nerve, such as tumor or skull fracture
21
Q
Facial Nerve Examination BP
A
A. Motor Status: test the facial muscles.
B. Reflexes: corneal(wink) conjunctiva and lid reflexes should be examined
C. Sensory Status: taste is tested as follows: sweet with sugar, sour with citric acid, bitter with quinine and salty
22
Q
BP
A
The examination should also include:
A full neurological examination
Ear and mouth examination to exclude Ramsey–Hunt Syndrome; Herpes zoster
Ear examination
23
Q
The most common is the HOUSE OF BRACKMANN for facial nerve grading: BP
A
Grade 1 (normal) *
Normal facial function in all area
Grade 2 (slight dysfunction) *
Gross: slight weakness noticeable on close inspection *
At rest: normal symmetry and tone
Motion: forehead-moderate to good function; eye-complete closure with minimum effort; mouthslight asymmetry
Grade 3(moderate dysfunction) *
Gross: obvious but not disfiguring difference between two sides; noticeable but not severe synkinesis, contracture and semi/hemi facial spasm *
Motion: forehead- slight to moderate movement; eye-complete closure with effort; mouth slight weak maximum effort
Grade 4(moderate severe dysfunction) *
Gross: obvious weakness and or/ disfiguring asymmetry
Motion: forehead-none; eye- incomplete closure; mouth- asymmetry with maximum effort
Grade 5 (severe dysfunction) *
Gross: only barely perceptible motion *
At rest: asymmetry *
Motion: forehead-none; eye-incomplete closure; mouth-slight movement
Grade 6 (total paralysis)
* No movement
24
Q
PROGNOSIS BP
A
- The extent of nerve damage determines the extent of recovery. With or without treatment, most individuals begin to get better within two weeks after the initial onset of symptoms and most recover some or all facial function within six months.
- Some individuals may show moderate to severe side effects. In some cases, residual muscle weakness may last longer or may be permanent.
- Taste returns before facial strength. If taste returns within five to seven days after symptoms began, it’s more likely you will recover completely.
- It’s also more likely you will recover completely if your facial muscles were not fully paralyzed at the most severe point of the illness.
25
Good Prognosis signs BP
* Recovery of taste in 1st week
* Recovery of sensory function (taste) before motor function. *
Recovery of motor function, usual order of function is:
o Buccinator
o Zygomatic
o Inferior Levator
o Orbicularis occuli
o Frontalis *
Incomplete paralysis in the 1st 5-7 days *
If within after few days’ onset, EMG shows there are motor units under voluntary control in the facial mm and from CN7 remains normal or only slightly slow *
Return of voluntary motor power at the end of 3 weeks from onset
26
FACTORS ASSOCIATED WITH A POORER DIAGNOSIS BP
* Age greater than 60 years
* Hypertension
* Hyperacusis
* Lacrimation has decreased
* Diabetes Mellitus
* impairment of taste and complete facial weakness
* After ten years, evidence of denervation suggests a long period of recovery, which is often incomplete.
27
MEDICAL MANAGEMENT BP
* Corticosteroids
* Prednisone
o The standard drug used in bell palsy, is a glucocorticoid medication mostly used to suppress the immune system and decrease inflammation.
Antiviral drugs
Acyclovir and valacyclovir
Have been administered in the treatment of bell palsy in combination with prednisone or have been used alone in patients who cannot take prednisone.
* Methylcellulose drops are used for affected eye
* Analgesics as required for pain
* Steroids to reduce edema of facial nerve
28
SURGICAL MANAGEMENT BP
Hypoglossal
o Facial nerve anastomosis to restore partial facial; Function if none has returned by 6-12 months
oFacial nerve grafting
o Facial nerve decompression
o Subocularis oculi fat lift
29
PHYSICAL THERAPY MANAGEMENT
for Bells Palsy
* Infrared rays and hot moist pack it has been recommended to use local superficial heat therapy for 15 minutes per session for the facial muscle prior to ES, massage or exercises, heat therapy improves local circulation and decrease skin resistance to ES, thus the lowest current intensity could be used.
* Electrical stimulation of the muscle aims to preserving muscle bulk especially in complete paralysis and it has also a physiological benefit as the patient observes muscle contraction in his face that gives him hope of recovery from facial paralysis.
*Facial massage improves circulation and may prevent contractures
Facial exercises with mirror for biofeedback- active exercise prevent muscle atrophy and improves muscle function
Sit relaxed in front of a mirror
Gently raise eyebrows, you can help the movement with finger
Draw your eyebrows together(frowning)
Wrinkle up your nose
Take a deep breath to your nose and flare nostrils
Gently try and move corners of mouth outwards
Try to smile and see if you can hold it
Lift 1 corner of the mouth and other
30
Is an autoimmune condition which attacks the myelin sheath of the neurons in the peripheral nervous system. The damage to the nerves causes the muscles to be weakened and sometimes paralyzed. This condition is idiopathic, the syndrome often follows infection with a virus or bacteria. GBS
GUILLAIN BARRE SYNDROME
31
This condition has many classifications and subtypes, namely: GBS
* Acute Inflammatory Demyelinating Polyneuropathy (AIDP)
- Weakness and paresthesia, this type may start progressing from your legs to the trunk and onto the rest of the upper extremities.
- Most common type.
- May also decrease you reflexes.
* Acute Motor Axonal Neuropathy (AMAN)
- Milder form of the condition
- non-inflammatory disease where the axons are the ones that are targeted by the body’s immune system.
- The myelin sheath not affected.
- Affects mostly children and young adults
* Acute Motor Sensory Axonal Neuropathy (AMSAN)
- Acute onset of weakness of the distal part, loss of DTR and sensorial symptoms.
- Mostly affects the adults
* Miller-Fischer Syndrome
-Rare form of GBS
-Primarily affects the eyes, making it difficult for the patient to move it.
- Damaged/impaired coordination of the limbs and unsteadiness.
-Absent of DTR
32
Nervous system outside the brain and spinal cord that is distributed to most parts of the body, and is responsible for motor and sensory activities (sensory receptors and motor/action conduction to the mm) and is divided into two parts. GBS
Peripheral Nervous system-
33
Parts of the PNS GBS
Somatic Nervous System- Regulates voluntary muscle movements.
Autonomic Nervous System regulates involuntary movement.
Neurons- Are nerve cells responsible for the conduction and relay of the information to and from the brain from the body and vice-versa, it also uses electrical signal impulses to deliver these messages and if stimulated can cause action potential.
34
Parts of the neuron GBS
Dendrites- Are flowerlike/ root-like structures that act as an input or receiving station of the neuron.
Cell body/Soma- Contains the nucleus and is spherical.
Axon- Acts as a bridge that is from the soma away to the distal part of the neuron that attaches to other neurons, where saltatory action happens (specifically in the myelin sheath on the axon), where impulses travel from the soma to the axon terminal to relay these messages.
-Myelin sheath- Made up of protein and fatty substances that envelops segments of the axon so that electrical impulses (saltatory conduction) travel faster, the thicker the myelin sheath the faster the conduction.
Synapse- A point where in two neurons come in contact with one another to receive or relay signals.
-
Schwann cell - produces myelin sheath in Peripheral Nervous System
Olegodendroctyes- Produces myelin sheath in the Central Nervous System.
35
Epidemiolog GBS
- Mostly affects Male than Females
- Distal parts are affected first
- Affects young adults to the middle-aged group ( 30 to 50 years of age)
36
EtiologyGBS
This condition is considered to be idiopathic.
- It is sometimes suspected to be caused by viral infection such as:
1. Respiratory infection (most common, usually appears after having this)
2. Gastrointestinal infection (most common, usually appears after having this)
3. Human Herpes Virus Infection
4. Mycoplasma pneumonia
5. Polio vaccination
6. Swine flu vaccine
7. Rabies vaccine
37
CLINICAL MANIFESTATION GBS
Classic Guillain-Bare Syndrome- begins with muscle weakness and diminished reflexes of lower extremities.
● Hyporeflexia and weakness progress and may result in quadriplegia.
● Demyelination of the nerves that innervate the diaphragm and intercostal muscles result in neuromuscular respiratory failure.
● Sensory symptoms include paresthesia’s of the hands and feet and pain related to demyelination of sensory fibers
38
Cranial nerve demyelination can result a variety of clinical manifestations: GBS
● Optic nerve demyelination may result in blindness
● Bulbar muscle weakness related to demyelination of the glossopharyngeal and vagus nerves results in an inability to swallow or clear secretions
● Vagus nerve demyelination results in autonomic dysfunction, manifested by inability of the cardiovascular system
● The presentation is variable and may include tachycardia, bradycardia, hypertension or orthostatic hypotension.
● The symptoms of autonomic dysfunction occur and resolve rapidly.
Guillain-Barre Syndrome does not affect cognitive function or level of consciousness. While the classic clinical features include areflexia and ascending weakness. There may be a sensory presentation with progressive sensory symptoms, an atypical axonal destruction, and the Miller-Fischer variant, which includes paralysis of the ocular muscles, ataxia and areflexia.
39
Signs and Symptoms of GBS:
The typical patient with GBS, which in most cases will manifest as acute inflammatory demyelinating polyradiculopathy (AIDP), presents 2-4 weeks following a relatively benign respiratory or gastrointestinal illness with complaints of finger dysesthesias and proximal muscle weakness of the lower extremities. The weakness may progress over hours to days to involve the arms, truncal muscles, cranial nerves, and muscle of respiration.
Common complaints associated with cranial nerve involvement in GBS includes the following:
● Facial droop (may mimic Bell’s Palsy)
● Diplopias
● Dysarthria
● Dysphagia
● Ophthalmoplegia
● Pupillary disturbances
40
Clinical phases of GBS:
. Tingling on hand and feet
II. Difficulty in raising from chair
III. Areflexia, weakness, decrease DTR
IV. Respiratory monitoring
V. Mechanical ventilation
VI. Recovery/ Full activity
41
Most patients complain of paresthesia, numbness or similar sensory changes. Paresthesia’s generally begin in the toes and fingertips, progressing upward but generally not extending beyond the wrists or ankles. Pain associated with GBS is most sever in the shoulder girdle, back, buttocks and thighs and may occur with even the slightest movements. The pain is often described as aching or throbbing in nature.
42
Autonomic changes in GBS include following:
Tachycardia
● Bradycardia
● Facial flushing
● Paroxysmal hypertension
● Orthostatic hypotension
● Anhidrosis and/or diaphoresis
● Urinary retention
43
Typical respiratory complaints in GBS include following:
Dyspnea on exertion
● Shortness of breath
● Difficulty swallowing
● Slurred speech
44
DIAGNOSIS
History and neurologic exam GBS
● Diagnosis is based on the clinical presentation. The required diagnostic criteria for GBS include progressive weakness of two or more limbs due to neuropathy, areflexia.
● A history of a viral illness in the previous few weeks suggest the diagnosis
● Progressive weakness, decrease sensation, decreased deep tendon reflexes.
Changes in vital capacity and negative inspiratory force are assessed to identify impending neuromuscular respiratory failure.
45
Gullain-Barre Syndrome Disability Score:
1- Healthy state
2- Minor symptoms and capable of running
3- Able to walk 10 m or more without assistance but unable to run
4- Able to walk 10 m across an open space with help
5- Bedridden or chair-bound
6- Requiring assisted ventilation for atleast part of the day
7- Dead
46
Diagnostic evaluation: GBS
● Lumbar puncture: elevated protein levels are detected in CSF evaluation, without increase in other cells.
● Electrophysiology studies: nerve conduction velocity shows decreased conduction velocity of peripheral nerves.
GBS is generally diagnosed on clinical grounds. A basic peripheral neuropathy workup is recommended in cases in which the diagnosis is uncertain. Biochemical screening can also be conducted and would include the following studies:
● Electrolyte levels
● Liver function test (LFTs)
● Creatine phosphokinase (CPK) level
● Erythrocyte sedimentation rate (ESR)
Needle EMG and nerve conduction studies
47
Signs of demyelination can include the following: GBS
● Nerve conduction slowing
● Prolongation of the distal latencies
● Prolongation of the F-waves
● Conduction block or dispersion of responses: evidence frequently demonstrated at sites of natural nerve compression
● Weak muscles showing reduced recruitment: demonstrated with needle examination (electromyography EMG)
48
Pulmonary Function: GBS
Maximal respiratory pressures and vital capacities are measurements of neuromuscular respiratory function and predict diaphragmatic strength. Maximal respiratory pressures also reflect abdominal muscle strength. Negative inspiratory force (NIF) is relatively easy beside test to measure respiratory muscle function. Normal is usually greater than 60 cm water. If the NIF is dropping or nears 20 cm water, respiratory support needs to be available.
49
Cerebrospinal fluid studies: GBSSS
Most, but not all, patients with GBS have an elevated cerebrospinal fluid (CSF) protein level (>400 mg/L), with normal CSF cell count. Elevated or rising protein levels on serial lumbar punctures and 10 or fewer mononuclear cells/mm3 strongly support the diagnosis.
50
Prognosis GBSS
Recovery can take weeks, months, or years. Most people survive and recover completely. In some people, mild weakness may persist. The outcome is likely to be good when the symptoms go away soon after they first started.
A poor prognosis with GBS is related to quadriparesis, the need for respiratory support, cranial nerve involvement, rapid progression, older age at onset, and a history of GI illness. Additionally, if the individual with GBS is older than 60 years old, achieves maximal deficits in less than 7 days, and needs ventilatory, he or she has less than a 20% chance of walking six months after onset of GBS.
51
Acute Motor Axonal Neuropathy= good prognosis
Acute Motor Sensory Axonal Neuropathy= poor prognosis
Miller-Fischer Syndrome= slow and incomplete recovery
52
MEDICAL MANAGEMENT FOR GBS
Each day counts; ~2 weeks after the first motor symptoms, it is not known whether immunotherapy is still effective
● Intravenous immunoglobin therapy - Prevents immune system from further attacking Schwann cells and myelin by blocking receptors on microphages
● Plasmapheresis - Filters blood plasma to remove antibodies and aids in replacing lost fluids
● Corticosteroids - Inhibit inflammation associated with symptoms
53
Surgical ManagemenT FOR GBS
● Tracheotomy- surgical opening of the trachea to provide and secure an open airway; respiratory
assistance
54
PT MANAGEMENT GBS
Acute Progressive Stage:
● PROM
● Bed mobility
Recovery Stage:
● PROM
● AROM
● Sensory education
● Includes occupational therapy, and supervised desensitization therapy to and able patients to tolerate practicing their daily living task like ADEPT.
● Providing ankle foot orthosis to prevent plantar contractures
● Improving endurance
● Strengthening different muscle groups
● Improving flexibility with progressive ambulation program that commencing with bed mobility techniques. Use of wheelchair for patients walking
● Parallel bars activities
● Using adaptive gait aids: walker, crutches, canes
● Functioning and weight lifting exercise- to develop UE strength and endurance
Re-conditioning:
● Breathing exercise
● Energy conservation techniques
Respiratory therapy
Maintenance of clear airway & prevention of lung infection
● The patient breathing will be assisted by intermittent positive pressure ventilation (IPPV) via a cuffed tracheostomy tube.
● Postural draining areas of lung tissues, 2-hourly turning onto supine and side lying positions.
● A suction catheter is used to remove secretions from respective passage until the cough reflex re-appears.
● Manual techniques like vibration with/without over pressure.
● 2-4 litre anaesthetic bag can be used to enhance chest expansion. Therefore, 2 people are necessary for this technique, one to squeeze the bag and another to apply chest manipulation.
● Rib springing to stimulate to cough.
● Introduce breathing and coughing exercises to maintain good airway exchange.
● After the removal of ventilator and adequate expansion, effective coughing must be taught to the patient.
● As neurons recover, active assisted or active breathing exercises may commence with good amount of relaxing time.
55
To maintain normal joint movement GBS
● Proper positioning
o Gentle passive movements through full ROM at least three times a day especially at hip, shoulder, wrist, ankle, feet.
● Maintenance of circulation
o Range of motion exercises
● Pain management
o Transcutaneous electrical nerve stimulator
● Muscle re-education
o Electrical stimulator
● Strengthening of muscles
o Progressive resistive exercises
o Isometric exercises
● Locomotion difficulties
o Parallel bars exercises
o Gait training
o Assistive devices
56
CEREBROVASCULAR DISEASE
refers to the large part of the brain—the cerebrum
“VASCULAR” which means arteries and veins
Together, the word cerebrovascular refers to blood flow in the brain. The term
cerebrovascular disease includes all disorders in which an area of the brain is
temporarily or permanently affected by ischemia or bleeding and one or more of the
cerebral blood vessels are involved in the pathological process. Restrictions in blood
flow may occur from vessel narrowing (stenosis), clot formation (thrombosis), blockage
(embolism) or blood vessel rupture (hemorrhage). Lack of sufficient blood flow
(ischemia) affects brain tissue and may cause a stroke.
Cerebrovascular ailment consists of quite a few scientific situations that have an effect
on the blood vessels of the mind and the cerebral circulation. Arteries offering oxygen
and vitamins to the mind are regularly broken or deformed in those disorders. The
maximum not unusual place presentation of cerebrovascular ailment is an ischemic
stroke or mini-stroke and on occasion a hemorrhagic stroke.
57
RELATED ANATOMY
THE BRAIN CVD
It is the control center for registering sensations, correlating them with one another and
with stored information, making decisions, and taking actions. It is also the center for
intellect, emotions, behavior, and memory.
a. Cerebrum- the largest part of the brain and consists of two cerebral
hemispheres– the Right and Left cerebral hemispheres. Generally, it performs
higher functions like interpreting touch, vision, hearing, speech, reasoning,
emotions, learning, and fine control of movement. The Left hemisphere functions
more for the academic and logical side of the brain. The Right hemisphere is
more on the artistic and creative side of the brain.
b. Cerebellum- Smoothens and coordinates contractions of skeletal muscles. It also
regulates posture and balance.
c. Brain Stem- the distal part of the brain that is made up of the midbrain, pons, and
medulla oblongata. It regulates breathing, heart rate, blood pressure, and several
other important functions
58
Cerebrovascular diseases can affect both arteries and veins. The most commonly
affected cerebral blood vessels that supply blood to your brain include:
● Carotid arteries: These blood vessels run along the front of your neck. The
carotid arteries transport oxygen-rich blood from the heart to the brain and head.
● Vertebral arteries: These blood vessels run along the back of your neck. They
carry blood to the brain and spinal cord,
The vertebral artery provides 20% of blood flow to your brain (the carotid artery supplies
the other 80%).
59
EPIDEMIOLOGY CVD
● Stroke is the fourth leading cause of death in United States
● Leading cause of long-term disability among adults in United States
● Women have a lower age-adjusted stroke incidence than men.
● However, this is reversed in older ages; Women: 85 years old > Men
● 28% of stroke occur in individuals younger than 65 years of age
● Of patients with stroke, hemorrhagic stroke > ischemic death, hemorrhagic with
mortality rates of 37% - 38%; ischemic with 8% - 12% at 1 month
● Atherosclerosis is a major contributory factor in cerebrovascular disease
60
ETIOLOGY CVD
Causes of cerebrovascular disease may include:
● Thrombosis: usually happens in areas where your blood vessel is narrow or
irregular.
● Embolism: The most common type of embolism is when a clot travels from your
heart to your brain.
● Blood vessel rupture (hemorrhage): usually occurs in conjunction with
uncontrolled high blood pressure
● Plaque build-up in the arteries (atherosclerosis) in your brain.
● Structural problems in your brain’s blood vessels.
● Traumatic brain injury (TBI).
61
RISK FACTORS - CVD
Overall, you’re at higher risk of cerebrovascular disease if you have:
You may be at higher risk of certain types of cerebrovascular disease if you:
● Pregnant, which increases your risk of cerebral venous thrombosis.
● Inherited (congenital) medical condition, which increases your risk of a brain
aneurysm, amongst other vascular conditions.
● Traumatic brain injury.
● Take hormone replacement therapy (HRT), which can increase your risk of
stroke if you have atherosclerosis or carotid artery disease.
● Smoking: Decrease risk by quitting smoking. Risk may be increased further with
the use of some forms of oral contraceptives and are a smoker. There is recent
evidence that long-term secondhand smoke exposure may increase the risk of
stroke.
● High blood pressure: Blood pressure of 140/90 mm Hg or higher is the most
important risk factor for stroke. Controlling blood pressure is crucial to stroke
prevention.
● Carotid or other artery disease: The carotid arteries in the neck supply blood to
the brain. A carotid artery narrowed by fatty deposits from atherosclerosis
(plaque build ups in artery walls) may become blocked by a blood clot.
● History of transient ischemic attacks (TIAs) Those who have had a stroke are
at much higher risk of having another one. Those who have had a heart attack
are also at higher risk of having a stroke.
● Diabetes: It is crucial to control blood sugar levels, blood pressure and
cholesterol levels. Diabetes, especially when untreated, puts one at greater risk
of stroke and has many other serious health implications.
● High blood cholesterol: A high level of total cholesterol in the blood (240 mg/dL
or higher) is a major risk factor for heart disease, which raises the risk of stroke.
● Physical inactivity and obesity: Being inactive, obese or both can increase the
risk of high blood pressure, high blood cholesterol, diabetes, heart disease and
stroke.
● Recent research shows evidence that people receiving hormone replacement
therapy (HRT) have an overall 29 percent increased risk of stroke, in particular
ischemic stroke.
Uncontrollable or Irreversible risk factors include:
● Age: People of all ages, including children, have strokes. But the older you are,
the greater your risk of stroke.
● Gender: Stroke is more common in men than in women.
● Heredity and race: There is a greater risk of stroke if a parent, grandparent,
sister or brother has had a stroke. Blacks have a much higher risk of death from
a stroke than Caucasians do, partly because they are more prone to having high
blood pressure, diabetes and obesity.
62
TYPES/CLASSIFICATIONS CVD
STROKE- is an abrupt interruption of constant blood flow to the brain that causes loss
of neurological function
Ischemic Stroke- occurs when a blood clot blocks or narrows an artery leading to the
brain
● Thrombotic Stroke- occurs when a blood clot, called a thrombus, block an artery
to the brain and stops blood flow
● Embolic Stroke- occurs when a piece of plaque or thrombus travels from its
original site and blocks an artery downstream
Hemorrhagic Stroke- rupture of an aneurysm or vascular malformation.
● Intracerebral Hemorrhage- occurs when there is bleeding directly into the brain
tissue
● Subarachnoid Hemorrhage- occurs when the bleeding fills the cerebrospinal fluid
spaces around the brain
Transient Ischemic Attack- Most likely an artery to the brain is temporarily blocked,
but the blockage dislodges before any permanent damage occurs
CAROTID STENOSIS- Plaque forms when the internal carotid arteries become blocked
by fat and cholesterol. Severe blockage is called carotid stenosis
CEREBRAL ANEURYSM- Develop at the point where a blood vessel branches. The
disorder may result from congenital effects
Vascular Malformation- refers to an abnormal connection of an artery, vein or both
63
CLINICAL MANIFESTATION CVD
● a severe headache
● paralysis of one side of the body
● weakness on one side
● confusion
● difficulty communicating
● losing vision on one side
● slurred speech
● trouble speaking
● balance problems
64
DIAGNOSIS CVD
● Cerebral angiography (also called vertebral angiogram, carotid angiogram)
- A catheter (a long, narrow, flexible tube) is inserted through the needle
and into the artery. It is then threaded through the main vessels of the
abdomen and chest until it is properly placed in the arteries of the neck.
This procedure is monitored by a fluoroscope (a special X-ray that projects
the images on a TV monitor).
● MRI (magnetic resonance imaging)
- A diagnostic test that produces three-dimensional images of body
structures using magnetic fields and computer technology. It can clearly
show various types of nerve tissue and clear pictures of the brainstem and
posterior brain
● Spinal tap (lumbar puncture)
- An invasive diagnostic test that uses a needle to remove a sample of
cerebrospinal fluid from the space surrounding the spinal cord. This test
can be helpful in detecting bleeding caused by a cerebral hemorrhage.
● Carotid duplex (also called carotid ultrasound)
- A water-soluble gel is placed on the skin where the transducer (a
handheld device that directs the high-frequency sound waves to the
arteries being tested) is to be placed.
● Computed tomography (CT or CAT scan)
- A CT scan is a useful diagnostic test for hemorrhagic strokes because
blood can easily be seen. However, damage from an ischemic stroke may
not be revealed on a CT scan for several hours or days and the individual
arteries in the brain cannot be seen.
● CTA (CT angiography)
- Allows clinicians to see blood vessels of the head and neck and is
increasingly being used instead of an invasive angiogram.
● Doppler ultrasound
- A water-soluble gel is placed on the transducer (a handheld device that
directs the high-frequency sound waves to the artery or vein being tested)
and the skin over the veins of the extremity being tested. There is a
"swishing" sound on the Doppler if the venous system is normal.
● Electroencephalogram (EEG)
- A diagnostic test using small metal discs (electrodes) placed on a person's
scalp to pick up electrical impulses. These electrical signals are printed
out as brain waves.
● Magnetic Resonance Angiogram (MRA)
- This is a noninvasive study which is conducted in a Magnetic Resonance
Imager (MRI). The magnetic images are assembled by a computer to
provide an image of the arteries in the head and neck. The MRA shows the actual blood vessels in the neck and brain and can help detect Blockage and aneurysms
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DIAGNOSTIC TEST CVD
● Glasgow Coma Scale
● Los Angeles Motor Scale (LAMS) for suspected stroke
66
DIFFERENTIAL DIAGNOSIS CVD
Definition Similarities Difference
Cerebral Palsy group of disorders that affect
movement and muscle tone or posture
● Manifest spastic paralysis
● Acquired lesions on motor areas of
cerebral cortex
● Damage to the immature brain
before, during or after birth.
● Traumatic injury to a developing brain.
● Infections could also cause damage to a developing brain. Traumatic
Brain Injury sudden injury that causes damage to
the brain. It may happen when there is a blow, bump, or jolt to the head
● Both conditions affect the BRAIN.
● Both can lead to cognitive, neurological and
Psychological disorders.
● They manifest motor and cognitive dysfunction.
● Seizures and Spasticity can occur in both conditions.
● TBI is an alteration in brain function, or other evidence of brain pathology, caused by an
external force.
● CVD is a NONTRAUMATIC BRAIN INJURY
caused by occlusion or rupture of cerebral blood vessels that result in sudden, focal neurological deficits
Bell’s Palsy- condition that causes a temporary weakness or paralysis of the muscles in the face
● Facial Paralysis or Weakness
● Bell’s Palsy
Paralysis/weaknes s on the entire
side of the face; Only affecting facial area; Lower Motor Neuron Lesion
● CVD
Paralysis/weaknes s to the lower face; Upper Motor Neuron Lesion
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PROGNOSIS CVD
Depends on the following factors:
● Extent of damage
● Age
● Health status
● Location of affectation
- Posterior circulation strokes are better than anterior circulation strokes
- Posterior circulation strokes are catastrophic due to the life support function of
the affected part (brainstem)
- Anterior circulation strokes are more extensive; has poor prognosis but less
complete
● Motivation and psychological status of patient
● Complications after onset
● Presence of risk factors
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Etiologic factor CVD
Thrombotic – severe impairment because infarction is extensive
Embolic – can trigger repeat stroke in the same area; poor prognosis
Lacunar – good prognosis because it involves small area
Hemorrhagic – poorest prognosis; often fatal
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MEDICAL MANAGEMENT CVD
● Improve cerebral perfusion by reestablishing circulation and oxygenation and
assist in stopping progression of the lesion to limit deficits.
● Maintain adequate blood pressure.
● Maintain sufficient cardiac output.
● Restore/maintain fluid and electrolyte balance.
● Maintain blood glucose levels within the normal range.
● Control seizures and infections.
● Control edema, intracranial pressure, and herniation using antiedema agents.
● Maintain bowel and bladder function, which may include urinary catheter.
● Maintain integrity of skin and joints.
● Decrease the risk of complications such as DVT, aspiration, decubitus ulcers,
and so forth.
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Medications Commonly Used to Treat Patients with Stroke
DRUG DESCRIPTION POSSIBLE ADVERSE
EFFECTS CVD
EFFECTS
Thrombolytics
(Alteplase [Activase or
tPA]) Converts plasminogen to
plasmin, degrades fibrin present
in clots, dissolves clots and
reestablishes blood flow
The most common
complication is bleeding and
brain hemorrhage
Anticoagulants
(e.g., warfarin
[Coumadin], heparin ,
dabigatran etexilate
[Pradaxa]):
Used to reduce the risk of blood
clots and prevent existing clots
from getting bigger by thinning
the blood.
Increased risk of bleeding
and hemorrhage, hematoma
Antiplatelet therapy
(e.g., acetylsalicylic
acid [aspirin])
Prevent platelets (blood cells)
from sticking together; long-term,
low-dose is used to decrease the
risk of thrombosis and recurrent
stroke; higher doses may be
used in place of anticoagulants
and may be recommended for
patients with atrial fibrillation.
Increased risk of gastric
ulcers and bleeding.
Antispastics
(e.g., baclofen
[Lioresal], dantrolene
sodium [Dantrium])
Used to relax skeletal muscle
and decrease muscle spasm.
May cause drowsiness,
dizziness, confusion,
weakness, among other
symptoms
Antidepressants
(e.g., fluoxetine
[Prozac], monoamine
oxidase inhibitors)
Used to control depression May cause anxiety, tremor,
insomnia, nausea
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SURGICAL MANAGEMENT CVD
Surgery may be indicated in:
● Patients with hemorrhagic stroke, to repair a superficial ruptured aneurysm or
AVM, prevent rebleeding, and evacuate a clot (hematoma).
● For resection of a superficial unruptured AVM when there is high risk of rupture
and stroke.
● Merci® Retriever System.
○ 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.
○ Patients who are not eligible for tPA or who do not respond to tPA may be
candidates for this surgical intervention
● The Penumbra System®
○ It uses a catheter and separator that is threaded to the site of the clot.
○ It suctions and grabs the clot and aspirates the site.
○ This system can be used effectively within an 8-hour window of symptom
onset.
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PHYSICAL THERAPY MANAGEMENT CVD
Acute Phase
Acute Phase
➢ Low-intensity rehabilitation starts as soon as the patient is medically stabilized,
usually within 72 hours.
➢ PT assists in ongoing monitoring of the patient’s recovery and is alert for
significant changes in the patient’s status.
➢ Early mobilization prevents or minimizes the harmful effects of bed rest and
deconditioning.
➢ Functional Reorganization on Hemiparetic Site
➢ Interventions include but are not limited to:
○ Positioning, functional mobility training (e.g., bed mobility, sitting, transfers,
locomotion), ADL training, range of motion (ROM), splinting, and
positioning➢ Patient and families/caregivers education.
Subacute Phase
➢ Patients with moderate or severe residual impairments or activity limitations may
benefit from intensive inpatient rehabilitation.
➢ If pt requires less intensive services, transfer to a transitional care unit (TCU).
Rehabilitation services are less intense here, ranging from 60 to 90 minutes of
therapy services 5 days per week.
➢ The timing of rehabilitation services is an important factor in predicting outcome.
Chronic Phase
➢ Generally more than 6 months post-stroke, typically delivered in an outpatient
rehabilitation facility, in a community setting, or at home.
➢ Interventions can be implemented including:
○ Constraint-induced movement therapy (CIMT)
○ Bilateral training
○ Virtual reality training
○ Electromechanical-assisted walking
➢ Patient and family education in home exercise program (HEP), importance of
maintaining exercise levels, health promotion, fall prevention, and safety.
➢ Patient should be assisted in resuming participation in community and
recreational activities.
➢ With increasing activity levels, PT should monitor the patient’s endurance levels
and provide instruction in activity pacing and energy conservation techniques as
needed.
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PHYSICAL THERAPY INTERVENTIONS INCLUDE: CVD
● Improve Motor Learning
○ Optimal motor learning can be promoted through attention to a number of
factors including
■ strategy development
■ Feedback
■ Practice
● Improve Sensory Function
○ Sensory retraining programs include use of
■ Mirror therapy
■ Repetitive sensory discrimination activities
● Improve Motor Learning
○ Optimal motor learning can be promoted through attention to a number of
factors including
■ strategy development
■ Feedback
■ Practice
● Improve Sensory Function
○ Sensory retraining programs include use of
■ Mirror therapy
■ Repetitive sensory discrimination activities
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● Interventions to Improve Hemianopsia and Unilateral Neglect CVD
○ Teach active visual scanning movements through turning of the head and
axial trunk rotation to the more involved side.
○ UE exercises that involve crossing the midline toward the hemiparetic side
are important.
○ Functional activities that encourage bilateral interaction are also valuable.
○ PT needs to maximize the patient’s attention by optimizing visual, tactile,
or proprioceptive stimuli on the more affected side.
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● Interventions to Improve Flexibility and Joint Integrity
○ Soft tissue/joint mobilization CVD
○ Soft tissue/joint mobilization and ROM exercises
○ ROM activities with terminal stretch
76
● Interventions to Improve Strength CVD
○ Progressive resistive strength training
○ Exercise modalities for strengthening
77
● Interventions to Manage Spasticity CVD
○ Early mobilization and daily stretching
○ Rhythmic rotation technique
○ Sustained stretching
○ PNF upper trunk patterns
○ Application of cold, massage, ES
78
● Interventions to Improve balance CVD
○ Balance Training
○ Postural strategy training
79
is a group of disorders that affect a person’s ability to move and maintain balance and
posture. CP is the most common motor disability in childhood. Cerebral means having to do with the brain. Palsy
means weakness or problems with using the muscles. CP is caused by abnormal brain development or damage to
the developing brain that affects a person’s ability to control his or her muscles.
Cerebral Palsy (CP)
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ANATOMY
CP affects the cerebral motor cortex. This is the part of the brain that directs muscle movement. The cerebral
cortex is composed of four lobes: frontal lobe, parietal lobe, temporal lobe, and occipital lobe. The major function
of the cerebrum is to control the voluntary muscular movements of the body. The cerebral cortex is mainly
involved in consciousness.
The cerebral cortex is the outer layer that lies on top of your cerebrum. Your cerebrum is the largest area of
your brain. Your cerebrum divides your brain into two halves called hemispheres. The hemispheres are attached
by a bundle of nerve fibers called the corpus callosum.
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EPIDEMIOLOGY
● In recent reports, the incidence has been estimated to be between 2.4 and 2.7 per 1000 live births. (Low
birth weight tiny neonates)
● The risk for CP in a child born full term is approximately 1 in 2000.
● CP was diagnosed in 12.3% of infants born at between 24 and 33 weeks of gestation.
1
● Approximately 50% of children with cerebral palsy have low birth weight and 28% weigh less than 1500 g
at birth.
● The incidence of cp in recent studies of multiple births is:
○ 9 to 12 per 1000 in twins
○ 31 to 45 per 1000 in triplets
○ 111 to 1000 in quadruplets
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ETIOLOGY
There have been multiple risk factors attributed to the development of CP. Although these identified risk factors
place children at higher risk for developing CP, the vast majority of children with risk factors do not develop CP.
83
Table 1: Risk Factors for Cerebral Palsy
PRENATAL:
Systemic disease during pregnancy
Brain abnormalities
Multiple Gestation Pregnancy
Assisted Reproduction Technology
Placenta Abnormalities
Premature rupture of membranes Neonatal Seizures
Oligohydramnios/Polyhydramnios Hyperbilirubinemia
Intrauterine Hypoxia
Intrauterine Infections
Potential Pathogenic genetic variants
PERINATAL:
Prematurity,CNS infections, i.e. viral
encephalitis, Bacterial
Meningitis , Stroke , Hypoxic-Ischemic Insults., Prolonged labor
POSTNATAL:
Head Trauma; Accidental/Non-Accidental, CNS infections, Infections, Stroke, Anoxic Insults, Neonatal Seizures, Hyperbilirubinemia
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Cerebral palsy is described based on the parts of the body it affects and the way it
affects movement.
CLASSIFICATION OF CEREBRAL PALSY
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By Body Part
1. QUADRIPLEGIA
● This type affects all four limbs — both arms and both legs. A person’s torso, facial, and oral
muscles are often affected, too.
2. TRIPLEGIA
● This type affects three limbs — one arm and both legs. A person’s torso, facial, and oral muscles
may be affected, too.
3. DIPLEGIA
● This type affects both legs. A person’s arms may be affected to a lesser extent.
4. HEMIPLEGIA
● This type affects one side of the body. People can either have right-side hemiplegia (affecting their
right arm and leg), or left-side hemiplegia (affecting their left arm and leg). Approximately 40% of
people with cerebral palsy have hemiplegia.
5. MONOPLEGIA
● This type affects only one limb.
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By Brain Injury Location
1. SPASTIC CEREBRAL PALSY
● Spastic cerebral palsy is the most common form, affecting up to 80% of people with CP.
● This type causes muscles to appear stiff and tight.
● This the result of damage to the motor cortex.
2. DYSKINETIC CEREBRAL PALSY
● Dyskinetic cerebral palsy — also known as athetoid cerebral palsy — occurs in 6% of people with
CP.
● This type is characterized by involuntary movements.
● This is the result of damage to the basal ganglia.
3. ATAXIC CEREBRAL PALSY
● Ataxic cerebral palsy occurs in 6% of people with CP.
● This type is characterized by shaky movements and affects a person’s balance and sense of
positioning in space.
● This is the result of damage to the cerebellum.
4. MIXED CEREBRAL PALSY
● Mixed cerebral palsy means that someone’s brain is injured in more than one location and they will
experience symptoms from multiple types of CP.
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GMFC (Gross Motor Function Classification) SYSTEM LEVELS FOR CHILDREN WITH CP BETWEEN AGES OF 6 & 12
YEARS
LEVEL I
- walks without restrictions; limitation in more advanced gross motor skills
LEVEL II
- walks without assistive devices; limitations in walking outdoors and in the community
LEVEL III
- walks with assistive mobility devices; limitations in walking outdoors and in the community
LEVEL IV
- self-mobility with limitations; children are transported or use power mobility outdoors and in community
LEVEL V
- self-mobility is severely limited even with use of assistive technology
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Levine's Diagnostic Criteria
● Posture and movement pattern
● Oral Motor Pattern
● Strabismus
● Tone of Muscle
● Evolutional Maldevelopment
● Reflex
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Types of cerebral palsy
There are 4 main types of cerebral palsy:
● spastic cerebral palsy
● dyskinetic cerebral palsy
● ataxic cerebral palsy
● mixed cerebral palsy
90
The main symptoms of cerebral palsy are problems with movement, coordination and development.
Possible signs in a child include:
● delays in reaching development milestones
● seeming too stiff or too floppy (hypotonia)
● weak arms or legs
● fidgety, jerky or clumsy movements
● random, uncontrolled movements
● muscle spasms
● shaking hands (intention tremors)
● walking on tiptoes
91
Classification according to Movements disorders:
● Spastic
● Athetoid
● Ataxic
92
Spastic
● Hypertonicity
● Most common (75% of all children with CP)
● Result of Upper Motor Neuron Involvement
● Retained primitive reflexes in affected areas of the body
Impact on motor function:
- Mild impairment - does not interfere with functional limits
- Severe - Inability to reach and grasp
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Ataxia/Ataxic
● Unsteadiness and difficulties with balance
● Involvement of Cerebellum
● Much less common
● Characterized by:
- Wide-based, staggering, unsteady gait
- Walk quickly (compensate for lack control and stability)
- Clumsy controlled movements
- Intention Tremors
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DIAGNOSIS
Assessment- Neurodevelopmental Treatment Approach Model of Assessment
● Data Collection
● Examination
● Evaluation
● Plan of Care
Diagnostic Imaging
● Magnetic resonance imaging (MRI) or computed tomography (CT) scan:
- provide evidence of hydrocephalus
- help determine the location and extent of structural lesions
- help rule out other conditions
● ECG - test used to evaluate the brain’s responses to external stimuli.
● Electromyogram (EMG) – where tiny needles are gently inserted into the muscles and nerves to check
how well they're working
Other test:
● blood tests - to check for problems that can cause similar symptoms to cerebral palsy
● Electroencephalogram (EEG) – where small pads are placed on the scalp to monitor brain activity and
check for signs of epilepsy.
● Single-photon emission tomography - experimental tool used to document cerebral perfusion.
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PROGNOSIS
Cerebral palsy life expectancy is generally calculated by the severity of a child’s condition. Mobility issues,
intellectual disabilities, vision/hearing impairments, and other coexisting conditions can all affect cerebral palsy
life spans.
Many children with milder forms of cerebral palsy have average survival times similar to those of the general
population.
Children with mild cerebral palsy have a 99% chance of living to 20 years old, whereas children with severe
cerebral palsy have a 40% chance, according to Dr. Ananya Mandal.(CEREBRAL PALSY GUIDE)
Generally, children born with cerebral palsy can expect to live between 30 and 70 years on average. Those
with the longest life expectancies usually have more mobility, better medical care and adaptive equipment and
greater autonomy and independence.
There is no cure for cerebral palsy and the condition lasts for life. However, unlike many other serious health
conditions, cerebral palsy does not worsen over time. This is because the condition is caused by a one-time brain
injury. Other co-mitigating factors and separate conditions not caused by the initial brain injury may impact
health and life expectancy over time. However, the majority of children diagnosed with cerebral palsy can expect
a relatively normal life expectancy.(NATIONAL INSTITUTES OF HEALTH)
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Orthopedic surgery
Orthopedic surgery (also spelled orthopaedic) is a type of surgery that is used to improve mobility. These
procedures are beneficial in treating spasticity, or jerky, exaggerated movements. This surgery is usually
suggested after previous therapies and medications have proven unsuccessful.
The 6 main types of orthopedic procedures are:
· Muscle lengthening
· Tendon lengthening
· Tendon transfer
· Tenotomy/myotomy
· Osteonomy
· Arthrodesis
97
Ambulatory
Ambulatory children with cerebral palsy may have a tendency to step mostly on their toes, cross their hips
while walking or bend their knees when taking strides. These issues can be caused by tight muscles, weakness, or
misalignment of the joints or bones.
98
Non-ambulatory
Non-ambulatory children are unable to walk, which is why the goal of orthopedic surgery is more centered
around increasing comfort and avoiding any further mobility complications.
99
Selective dorsal rhizotomy
Selective dorsal rhizotomy (SDR) is an aggressive procedure that helps reduce pain and spasticity. SDR is
typically recommended in severe cases of spasticity when other treatments have failed to make an impact.
Children with spasticity in the legs (spastic diplegia) tend to benefit more than children with spasticity in other
locations (quadriplegia, hemiplegia).
Selective dorsal rhizotomy improves:
· Walking
· Sitting
8
· Standing
· Balance
· Deformities in tendons, muscles, feet and hips
· Voluntary movement
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MEDICAL MANAGEMENT
Botulinum toxin
Upper motor neuron syndrome often leads to common patterns of motor dysfunction and characteristic
spasticity and contractures. Botulinum toxin (Botox) is a formulation of botulinum toxin type A, derived from the
bacterium Clostridium botulinum. This bacterium produces a protein that blocks the release of acetylcholine and
relaxes muscles.
Baclofen (Lioresal)
The AACPDM Treatment Outcomes Committee Review Panel’s systematic literature review in 200030
evaluated the use of intrathecal baclofen for spastic and dystonic cerebral palsy. Summary results reported
limited evidence for reduced spasticity in the lower extremities, with unclear effects for upper extremities.
101
PHYSIOTHERAPY MANAGEMENT OF CHILDREN WITH CP
Physiotherapist as an expert in the management of impairments seen in CP use different approaches as
identified by Patel.
102
PT Management Approaches
Neurodevelopmental technique (NDT), neuromuscular electrical stimulation, exercise therapy, hydrotherapy,
body weight support treadmill training, patterning, conductive education, constraints induced therapy, Vojta
method, and suit therapy.
103
The NDT approach
This approach was developed by mere personal observations of two individual Berta and Karel while
managing children with CP.[38] This technique was based on the assumption of Bobath that the motor
abnormalities in children with CP are as a result of delayed milestones or abnormal development of postural
control and reflexes because of the nervous system dysfunction.
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Body weight support treadmill training
This technique works primarily on eliciting and improving the stepping movement that is normally present in
newborn and infant even before the infant starts to bear weight, stand, or walk as the child attempts to walk on a
slowly moving treadmill with close monitoring and support.
105
CONVENTIONAL EXERCISE THERAPY
This encompasses the treatment regimen which includes passive movement, progressive resisted exercises,
passive stretching, weight bearing exercises, and progressive habilitation exercises.
106
Sensory integration training
Sensory integration was developed by an occupational therapist, Jean Ayres, in the 1960s.] In this concept,
difficulties in planning and organizing behavior are attributed to problems of processing sensory inputs within the
central nervous system, including vestibular, proprioceptive, tactile, visual, and auditory.
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CIMT
This is specifically used to improve the upper limb function in children with hemiplegic type of CP and the
sub-type that account for approximately 30% of all children with CP. The CIMT aims to increase spontaneous use
of the impaired arm by forcing the child to use it by restraining the other one, and it is characterized by
restraining of the unaffected side, concentrated and intensive practice, and shaping activities.
