Neurological Physical Therapy: Handbook of
Neurological Physical Therapy: Handbook of
Neurological Physical Therapy: Handbook of
Neurological
Physical Therapy
Evidence-Based Practice
Foreword
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Mission
This edition, will be useful to Physical Therapy students, Interns,
Medical students, Faculty, Nurse practitioners, Occupational
therapists, Physiatrist and physicians Assistant’s will find the
descriptions of diagnostic and Physical therapy management with
citations to the current literature useful in day-to-day patient care.
Outstanding Features
• Concise, clear presentation of the latest scientific facts, models
and methods of practice.
• More than 93 Indian Patients clinical photo gallery.
• Details presentation of all chapters including Neurological
examination, Neuroradiology imaging, Physical therapy in Bell’s
palsy, Stroke physical therapy, Parkinson’s disease, Spinal cord
injury Rehabilitation, Cerebral palsy, Cerebellar ataxia, and
Orthotics in neurological Rehabilitation.
• Recent references, articles, abstracts, and full further editions in
writing or via electronic e-mail. The author e-mail address:
shanmugampt@rediffmail.com
P Shanmuga Raju
Acknowledgments
CTION
ODUCTION
ODU
INTRODU
1
The human somatic cell is diploid with 46 chromosomes
(i.e. 23 pairs of chromosomes) of which 22 pairs are autosomes and
Neurological
one pair of sex chromosome (XX in female and XY in male). The
germ cells or gametes are haploid cells (i.e. 23 chromosomes). During
Examination
fertilization the male and female gamete unite to form the zygote
(diploid).
The zygote formed undergoes mitosis repeatedly to form the
embryo which later develops into an organism. Thus, all somatic
cells in a multicellular organism are descendants of one original
cell, the fertilized egg or zygote. Mitosis produces two daughter cells
per cycle and their genetic content is identical to mother cell.
Gametogenesis (formation of gametes) occurs only in specialized
cells (germ line) of the reproductive organs (gonads). In human, the
testes are male gonads and the ovaries are female gonads. Gamete
cells are produced through the process of mitosis. Mitosis consists
of two specialized, consecutive cell divisions in which the
chromosome number of resulting cells is reduced from a diploid
(2n) to a haploid (n) number. The number of chromosomes must be
reduced by half during gametogenesis in order to maintain the
chromosome number and characteristic of the species after
fertilization.
2 Handbook of Neurological Physical Therapy
NEUROLOGICAL EXAMINATION
The Neurological Examination as commonly done includes the
important elements such as the mental status, cranial nerves, motor
and sensory reflexes, cerebellar function, coordination, gait and
station, and other signs.
Social History
• Occupational and educational history/life style
• Personal habits (tobacco, alcohol).
Family History
• The family history is often of great importance
• Since many disorders of the central nervous system are hereditary
• The number of children and the occurrence of miscarriage and
still births should be assessed.
Neurological Examination
Assess Behavior
• Determine level of confusion, stupor, coma, delirium
• Glasgow Coma Scale (GCS): This scale is utilized to determine
Neurological Examination
Memory
• Assessment of memory is the most important component of
mental status testing.
Classification of Memory
• Immediate memory
• Recent memory (short-term memory)
• Remote memory (long-term memory).
Immediate Memory
• Is a very short function?
Neurological Examination 5
Recent Memory
• The patient to recall of recent information such as her address,
phone number, and how to come to the present building.
Remote Memory
• Memory of past events, i.e. birth dates of their children and grand
children, where did they grow up.
Attention
• Assess length of attention span, i.e. digit span retention test,
recall of up to 7 members in order presented.
• Assess time on task, frequency of redirection.
Emotional Response
• The patient is anxious, excited, depressed, frightened, apathetic
or euphoric.
disease.
• Sustained deep breathing
– Midbrain lesions, e.g. tumors, infarction, compression due to
herniation
• Irregular breathing
– Clustered breathing, gasping, or jerking inspiration
– Medullary lesions
– Indicating disturbance of the medullary inspiratory and
expiratory neurons.
Strength Scales
• Medical Research Council (MRC) scale (grade 0-5) (Table 1.1)
• Manual Muscle test (MMT) (Table 1.2)
• Clinically to evaluate muscle strength adequately without
resorting to special equipment:
– Dynamometers
– Myometers
– Ergometer
Upper extremity
Abduction of shoulders C5
Adduction of shoulder C5
Flexion of shoulder C5
Extension of elbow C7
Flexion of wrist C6, 7, 8
Extension of wrist C6, 7
Finger movements C8, T1
Lower extremity
Flexion of hip L1, 2, 3
Extension of hip L5, S1
Adduction of hip L5, S1
Flexion of knee L4, 5, S1, 2
Extension of knee L3, 4
Dorsiflexion of foot L4, 5
Plantar flexion S1
Inversion of foot L4
Eversion of foot L5, 6
Dorsiflexion of toes L5
Methods
• Inspection
• Muscle palpation
• Passive manipulation—to assess the extensibility, flexibility and
range of motion
• The limb is moved passively, first slowly and through a complete
range of motion, and then at varying speeds.
12 Handbook of Neurological Physical Therapy
Fig. 1.7: Test muscle tone: Flaccid paralysis/No response, usually complete
flexed at the right wrist (Hand drops). Left wrist is in normal position.
Neurological Examination
Fig. 1.8: Right knee in complete flexed pattern/left lower limb is normal.
Neurological Examination 13
Examination
• Inspection
• Palpation
• Measurement ( Tape Measure or Calipers)
• Muscle atrophy (Amyotrophy) - Decrease in muscle volume or
Bulk.
– Changes in shape or contour.
• Muscle hypertrophy—An increase in the bulk or volume of muscle
tissues.
Indications
Neurological Examination
• Muscle atrophy (Figs 1.9 and 1.10)
– E.g.: Diseases of anterior horn cells, root or peripheral nerve
– Congenital Hemiplegia
– Myogenic atrophy
• Neurogenic atrophy:
– E.g.: Bell's palsy or peripheral nerve injury
– Amyotrophic lateral sclerosis
– Progressive spinal muscular atrophy
– Peroneal muscular atrophy
– Muscular dystrophy, pseudo hypertrophy.
Example
Neurological Examination
Reflex Score
0 Absent
1 Decreased reflex
2 Normal response
3 Exaggerated
4 Hyperactive Neurological Examination
Fig. 1.11.B:
Knee jerk
Neurological Examination
Fig. 1.11C:
Biceps jerk
Fig. 1. 11D:
Supinator jerk
Neurological Examination 17
Plantar Response
• Applying a firm pressure along the lateral border of the dorsum
of the foot and observing the metatarsophalangeal joint of the
great toe
• In normal circumstance the toe flexors (goes down)
• In pyramidal and corticospinal lesions (upper motor neurone)
the great toe shows an extensor response (it goes up, with an
associated fanning of the toes)
• Babinski sign: Great toe extension (S1-2) Figs. 1.12 and 1.13
• Positive Babinski is an abnormal response to plantar reflex
testing.
Neurological Examination
Reflexes Tested
Primitive/Spinal
• Flexor withdrawal
• Crossed extension
• Traction
• Grasp.
Neurological Examination
Tonic/Brain Stem
• Asymmetrical tonic neck reflex (ATNR)
• Symmetrical tonic neck reflex (STNR)
• Symmetrical tonic labyrinthine reflex (STLR)
• Positive support, associated reactions.
Score
Scale range from
0 absent
1 Tone change; no visible movement of extremities
2+ Visible movement of extremities
3+ Exaggerated, full movement of extremities
4+ Obligatory and sustained movement, lasting for more than 30
seconds.
Neurological Examination 19
• C2 - Occipital
• C3 - Lateral Cervical area
• C4 - Tip of Scapula
• C5 - Lateral aspect of elbow
• C6 - Thumb
• C7 - Middle finger
Contd...
20 Handbook of Neurological Physical Therapy
Contd...
• C8 - Little finger
• T1 - Inner aspect of elbow
• T3 - Axilla
• T8 - Costal region
• T10 - Umbilicus
• T12 - Pubis
• L1 - Below Inguinal ligament
• L3 - Knee
• L4 - Medial surface of tibia
• L5 - Outer aspect of tibia to inner aspect of foot and great toe
• S1 - Lateral aspect of foot and little toe.
Two-Point Discrimination
• Test by placing two points of stimulus on the patients skin and
gradually bringing them together until there is one-point stimulus
• The patient is asked to determine if there is one point or two
points and when they come together to one point.
Barognosis
• Test by placing an object in the patient's hand and requesting
the patient to respond if it is heavier or lighter than the previous
object.
Texture
• Test by placing different textures sample cotton, wool, silk or
leather in the patients hand and asking the patient to identify
the texture.
Neurological Examination 21
Kinesthesia
• Moving the patient's extremity up, down, out or in. The patient
is asked to describe the movement by the therapist.
TESTING OF COORDINATION
Finger to Nose Test
• The patient extends the arm completely and then touches the tip
of the index finger to the tip of the nose, slowly at first, then
rapidly, with the eyes open and then closed
• If the patient is not fluent, then you should ask him/her to repeat
the action of touching his/her nose with the eyes closed
• Example: Cerebellar disease.
Heel-to-Shin Test
• To assess lower limb coordination
• Ask the patient to slide the heel of one foot in a straight line
down the shin of the other leg
• In cerebellar ataxia, the heel wavers across the intended target.
Dysdiadochokinesia
• Dysdiadochokinesia is an inability to perform rapidly repeated Neurological Examination
movements
• Test: Ask the patient to pretend to screw a light bulb into a socket
• Another test is to ask the patient to perform simple repetitive
movements , such as drawing a circle with a finger on the back of
one and then the other
• Slow, awkward movements indicate dysdiadochokinesia.
Romberg's Test
• A simple test to determine whether an ataxic gait (a patients's
unsteadiness) results form a cerebellar or proprioception lesion
• The patient is asked to stand with feet together and then to close
his/her eyes
• Where there is loss of proprioception, the patient immediately
loses stability (Positive Romberg's Test).
22 Handbook of Neurological Physical Therapy
GAIT ASSESSMENT
Methods
• Observation
• Gait analysis and Motion Lab
• EMG Biofeedback
• Assess length of step, width of base
• Abnormal leg movements
• Instability
• Associated postural movements.
BIBLIOGRAPHY
• Adams RD, Victor M. Principles of Neurology, New York: Mc-Graw
Hill, 2008.
• Brain Wr. Diseases of the nervous system; Oxford University press,
London, 1933; p. 899.
• Ballinger A, Patchett S. Clinical medicine, China, 3rd: Saunders, Elsevier,
2005; p. 635-720.
• Carr JH, Shepherd RB. Physiotherapy Disorders of the Brain. London,
Heineman, 1990.
• Donagly M, Neurology. Oxford Press, 2004.
• Fuller G. Neurological Examination Made easy. Edinburg: Churchill
Livingstone, 2006.
• Gajdosik RL, Bohannon RW. Clinical Measurement of Range of motion:
Neurological Examination
CTION
ODUCTION
ODU
INTRODU
2
The human somatic cell is diploid with 46 chromosomes
(i.e. 23 pairs of chromosomes) of which 22 pairs are autosomes and
Neuroradiology
one pair of sex chromosome (XX in female and XY in male). The
germ cells or gametes are haploid cells (i.e. 23 chromosomes). During
Imaging
fertilization the male and female gamete unite to form the zygote
(diploid).
The zygote formed undergoes mitosis repeatedly to form the
embryo which later develops into an organism. Thus, all somatic
cells in a multicellular organism are descendants of one original
cell, the fertilized egg or zygote. Mitosis produces two daughter cells
per cycle and their genetic content is identical to mother cell.
Gametogenesis (formation of gametes) occurs only in specialized
cells (germ line) of the reproductive organs (gonads). In human, the
testes are male gonads and the ovaries are female gonads. Gamete
cells are produced through the process of mitosis. Mitosis consists
of two specialized, consecutive cell divisions in which the
chromosome number of resulting cells is reduced from a diploid
(2n) to a haploid (n) number. The number of chromosomes must be
reduced by half during gametogenesis in order to maintain the
chromosome number and characteristic of the species after
fertilization.
24 Handbook of Neurological Physical Therapy
• Plays vital role in accident and emergency cases where its ability
to produce high quality images with minimal disturbance to
patient is particularly valuable
• Modality of choice for imaging acute head trauma—
Hemorrhages, contusions, Facial- Clavicle fractures
• In identifying calcified primary brain tumors, extra axial tumors
in adults, metastasis
• Best evaluation in fractures of spine
• In axial back pain, injection of contrast materials into nucleus of
intervertebral disc followed by CT Discography
• Use to imaging osseous structures of the spine, skull base and
temporal bones (William PD, 2001).
Neuroradiology Imaging 25
Myelography
• Radiography of spine following injection of an opaque substance
into the lumbar spinal subarachnoid space, usually at the L2- L3
• For diagnosis of diseases of the spinal cord and canal (e.g.
Syringomyelia, Paraplegia
• Evaluation of suspected meningeal or arachnoid cysts and the
localization of spinal dural arteriovenous fistulas and CSF
fistulas Neuroradiology Imaging
• Contraindications: Post Headache, vomiting and meningitis.
Ventriculography
• X-ray of skull following injection of air into lateral ventricles
• Useful with to increased intracranial pressures.
Angiography
• Evaluation of patients with vascular pathology
• Indication: For patients intra cranial small vessel pathology (such
as vasculitis) aneurysms, and vascular malformations
• Complications: atherosclerosis, vasospasm, low Cardiac output
and subarachnoid hemorrhage.
26 Handbook of Neurological Physical Therapy
Electromyography (EMG)
• EMG the recording of electrical changes present in muscles at
rest or evoked by voluntary movement
• The record is made by introducing a concentric needle into the
muscle to be tested
• When a normal muscle is completely relaxed, no electrical activity
can be detected in it.
Neuroradiology Imaging
Indication
• Lesions of the lower motor neuron
• Myotonia, myasthenia gravis
• Measure recovery after a peripheral nerve lesion
• It is useful in the diagnosis of neuromuscular diseases such as
motor neuron disease, muscular dystrophy and poliomyelitis.
Evoked Potentials
• External, auditory or somatosensory stimuli are used to evoke
potentials in brain
• Visual evoked potential (VEP)
• Brain auditory evoked potential (BAEP)
• Somatosensory evoked potential (SEP)
• Potentials are recorded by from surface electrodes and processed
by computer
• Delineates conduction times along there sensory pathways
• Detects lesions if responses are delayed or absent.
Muscle Biopsy
• The Chief use is to detect inflammatory myopathies particularly
in inflammatory disorders such as polymyositis, degenerative
disorders such as the muscular dystrophies (Dubowitz and
Brooke 1973)
• Help to identify a neurogenic atrophy by the uniformity of enzyme
activity in the reinnervated fibers
• The biopsy is taken from an affected muscle and then processed
for light and electron microscopy
• Use to identify the different muscle fiber types and abnormalities
in specific enzyme pathways.
28 Handbook of Neurological Physical Therapy
BIBLIOGRAPHY
• Adams RD, et al. Principles of Neurology. 5th ed, Newyork; Mc
Graw-Hill, 1997.
• David O. Wiebers, et al. Mayo Clinic Examinations in Neurology.
7th ed, Mosby, 1998; p. 331- 511.
• Dillon WP. Neuroimaging in Neurologic Disorders, Mc Graw-
Hill, New York, 2001; p. 2337-41.
• Donaghy. M. Brain's Diseases of the Nervous System. 11th ed,
Oxford University press, 2001.
• Fuller G. Neurological Examination made easy. Newyork;
Churchill Livingstone, 1999.
• Frackowiak, RSJ. Positron emission tomography in neurology.
In Recent advances in Clinical neurology. vol. 5; Edinburgh,
Churchill Livingstone, 1988; p. 239-77.
• Gilliatt. RW. Clinical Electromyography in Modern trends in
Neurology, Willams, London, 1957; p. 65.
• Hill.D. Encephalography in Recent Advances in Neurology and
Psychiatry, ed Brain WR and Strauss EB, 6th ed, London, 1995;
113-14.
• Kimura J. Electro Diagnosis in Diseases of Nerve and Muscle,
2nd ed, Philadelphia, Davis, 1989.
• Susan B.O' Sullivan. Neurological Physical Therapy. APTA;
Neuroradiology Imaging
CTION
ODUCTION
ODU
INTRODU
3
The human somatic cell is diploid with 46 chromosomes
(i.e. 23 pairs of chromosomes) of which 22 pairs are autosomes and
Physical Therapy
one pair of sex chromosome (XX in female and XY in male). The
germ cells or gametes are haploid cells (i.e. 23 chromosomes). During
in Bell’s Palsy
fertilization the male and female gamete unite to form the zygote
(diploid).
The zygote formed undergoes mitosis repeatedly to form the
embryo which later develops into an organism. Thus, all somatic
cells in a multicellular organism are descendants of one original
cell, the fertilized egg or zygote. Mitosis produces two daughter cells
per cycle and their genetic content is identical to mother cell.
Gametogenesis (formation of gametes) occurs only in specialized
cells (germ line) of the reproductive organs (gonads). In human, the
testes are male gonads and the ovaries are female gonads. Gamete
cells are produced through the process of mitosis. Mitosis consists
of two specialized, consecutive cell divisions in which the
chromosome number of resulting cells is reduced from a diploid
(2n) to a haploid (n) number. The number of chromosomes must be
reduced by half during gametogenesis in order to maintain the
chromosome number and characteristic of the species after
fertilization.
30 Handbook of Neurological Physical Therapy
BELL'S PALSY
Sir Charles Bell (1821) described the Facial (Bell's) Palsy. It is a
complex neuromuscular facial disorder or unknown etiology
commonly affecting the motor neurons of facial muscles receiving
their neurological innervations from the seventh cranial nerve
(Vanswearinggen and Brach 1998).
Etiology
• Cold exposure is a frequent cause, for example driving with a car
window open in frigid weather or sleeping with window open a
chilly night
• Inflammation and edema
• Herpes Zoster Virus (HZV)
• Facial Trauma (e.g. Obstetric forceps)
• Ramsay Hunt syndrome
• Postacoustic neuromas surgery
• Some cases have recently being reported after inflammation of
intranasal influenza vaccine.
Incidence
Physical Therapy in Bell’s Palsy
Diagnosis
EMG Test
• The severity and the extent of nerve involvement and the presence
of nerve damage is determined.
X-Ray
• Can help rule out infection or tumor.
MRI/ CT scan
• Can eliminate other causes of pressure on the facial nerve.
Special Tests
• Facial nerve grading system (House JW, Brackmann DE, 1985)
(Table 3.1)
Assessment
• Observe for drooping of mouth, eyelid's that don't close
• Assess function of facial muscle expression (wrinkle forehead,
raised eyebrows, frown, smile, close eyes, tightly puff checks)
• Assess taste of the anterior 2/3rd of tongue.
Physical Therapy in Bell’s Palsy
Table: 3.1: House -Brackmann Facial Nerve Scale, 1985
Contd...
34 Handbook of Neurological Physical Therapy
Contd...
Grade Description Findings
Aims
• To educate/reassure the patient about the condition
Physical Therapy in Bell’s Palsy
Patient Education
• Explain the condition to the patient; its cause, incidence,
prognosis and treatment
Physical Therapy in Bell’s Pasly 35
Electrothermotherapy
Electrical Stimulation (ES)
• ES of paralyzed muscles has long been a popular intervention
for patients with Bell's palsy
• Six facial muscles (Frontalis, Orbularis oculi, Oribularis oris,
Zygomaticus major, Nasalis and Triangularis)
• Pulsed electrical stimulation to reduce neuromuscular
conduction latencies and minimize clinical impairments in
patients with by standing facial nerve damage (Farragher, et al)
• To improve motor recovery in patients with acute and chronic
Bell's palsy (Patrica JO and Michelle Lz, et al. 2006).
EMG Biofeedback
• EMG Biofeedback is more effective and significantly improved
symmetry of voluntary movement and linear measurement of
facial expression (Ross. et al. 1991).
Laser
• Laser, still has no study supporting to use it with acute or chronic
condition.
the patient can observe the angle, strength and speed of each
movement, because rapid movements can't help the patient in
controlling the abnormal movement (synkinesis).
Stretching
• Stretching is recommended here to prevent muscle tightness.
Facial Manipulation
• Facial manipulation can be performed in conjunction with other
treatment options. It can be done to improve perceptual
awareness
• Facial manipulations on the face include:
– Effleurage
– Finger or thumb kneading
– Wringing
– Hacking
– Tapping
– Stroking.
Physical Therapy in Bell’s Pasly 37
Kabat Rehabilitation
• Kabat techniques are a type of motor control rehabilitation
technique based on Proprioceptive neuromuscular facilitation
(PNF)
• During Kabat, therapist facilitate the voluntary contraction of
the impaired muscle by applying a global stretching then resis-
tance to the entire muscular section and the motivate action by
verbal input and manual contact
• Prior to Kabat, ice stimulation has to perform a specific muscular
group in order to increase its contractile power (Barbara et al.
2010).
BIBLIOGRAPHY
• Adour KK, Ruboyianes JM, Trent CS, et al. Bell's Palsy treatment with
acyclovir and prednisone with compared with prednisone alone: A
double blind, randomized controlled trial; Ann Oto Rhin and Largng
vol:105; Issue, 1999;5:371-8.
• Brach JS, Vanswearingen JM. Not all facial paralysis is Bell's palsy: A
Case report. Arch Phys Med Rehab, 1999;80:857-9.
• Buttress S, Herren K. Electrical stimulation and Bell's palsy (Best
evidence Topic Report). Emerg Med J; 2002;19: 428.
• Barbara, Maurizo, et al. Role of Kabat Physical rehabilitation in Bell's
palsy, Acta Oto Laryngoloica, No: 1, March , 2010; 130: 167-72 (6).
• Cronin GW, Steenerson RL. The Effectiveness of Neuromuscular facial Physical Therapy in Bell’s Palsy
retraining combined with electromyography in facial paralysis
Rehabilitation. Otolaryngology. Head and Neck surgery, 2003;128:
p 534-8.
• Centre for Reviews and Dissemination: The efficacy of electrotherapy
for Bell's Palsy: A systemic review (Provisional Record). Database of
abstracts of Reviews of effectiveness, 2005; issue: 4.
• Diels HJ. Facial Paralysis: is there a role for a Therapist. Facial Plast
surg, 2000;16: p 361-4.
• Dalla T, Elena, Bossi, Daniela, et al. Usefulness of BFB/EMG in facial
Palsy Rehabilitation. Disab and Rehab, 2005; Vol:27, No: 14: p. 809-15.
• Elisabet CW, Monika FO, Per H, Ingemer F. Evaluation of a Physio-
therapeutic treatment intervention in Bell's Palsy. Physio Ther Pract,
2006; vol 22 (no:1): p. 43-52.
• Farragher D, Kidd GL, Tallis R. Eutrophic Electrical stimulation for
Bell's palsy. Clinical Rehabilitation; 1987;1:265-71.
• Fernado CK, Basmajian JV. Biofeedback in Physical medicine and
rehabilitation, Biofeedback and self Regulation. Task Force Report of
BSA; 1978; vol 3 (no: 4).
38 Handbook of Neurological Physical Therapy
CTION
ODUCTION
ODU
INTRODU
4
The human somatic cell is diploid with 46 chromosomes
(i.e. 23 pairs of chromosomes) of which 22 pairs are autosomes and
Stroke Physical
one pair of sex chromosome (XX in female and XY in male). The
germ cells or gametes are haploid cells (i.e. 23 chromosomes). During
Therapy
fertilization the male and female gamete unite to form the zygote
(diploid).
The zygote formed undergoes mitosis repeatedly to form the
embryo which later develops into an organism. Thus, all somatic
cells in a multicellular organism are descendants of one original
cell, the fertilized egg or zygote. Mitosis produces two daughter cells
per cycle and their genetic content is identical to mother cell.
Gametogenesis (formation of gametes) occurs only in specialized
cells (germ line) of the reproductive organs (gonads). In human, the
testes are male gonads and the ovaries are female gonads. Gamete
cells are produced through the process of mitosis. Mitosis consists
of two specialized, consecutive cell divisions in which the
chromosome number of resulting cells is reduced from a diploid
(2n) to a haploid (n) number. The number of chromosomes must be
reduced by half during gametogenesis in order to maintain the
chromosome number and characteristic of the species after
fertilization.
40 Handbook of Neurological Physical Therapy
STROKE
The term of Stroke (or) Cerebrovascular Accident (CVA) is a sudden
focal neurologic deficit resulting from ischemic or hemorrhagic lesion
in the brain (O'sullivan 2004). Approximately 80% of strokes are
caused by to little blood flow (ischemic stroke) and the remaining
20% are nearly equally between hemorrhage into brain tissue
(parenchymatous hemorrhage) and hemorrhage into the
surrounding subarachnoid space (Subarachnoid Hemorrhage).
CEREBROVASCULAR ANATOMY
Most of strokes caused by abnormalities with in the cerebral
circulation, an understanding of cerebrovascular anatomy helps in
arriving at the correct diagnosis and determining the underlying
pathogenesis and prognosis.
The brain is supplied by four major arteries:
1. The left and right internal carotid artery and vertebral arteries.
2. The left common carotid artery arise from aortic arch, but the
other vessels originate from branches of the aorta.
3. The right common carotid artery.
4. The left and right vertebral arteries.
Stroke Physical Therapy
Epidemiology
• Third leading cause of death (1 of every 14.5 deaths after heart
disease and cancer in world wide)
• 72% of strokes occur in patients occur in patients > 65 years of
age
• 14% of patients have a transient ischemic attack (TIA) within
one year
• 50-70% of stroke survivors regain functional independence,
whereas 15-30% are permanently disabled (Brammer CM, et al
2002).
Classification
• Transient Ischemic Attack (TIA): An acute loss of focal cerebral
or monocular function with symptoms lasting less than 24 hours
Stroke Physical Therapy 41
RISK FACTORS
• Hypertension
• Cardiac disease
• Age
• Gender (Male/Female)
• Diabetes Mellitus
• Family History
• Smoking
• Alcohol
• Increased hematocrit
• TIA
• Elevated fibrinogen level Stroke Physical Therapy
• Hemoglobinopathy.
PATHOPHYSIOLOGY
• Cerebral Ischemia defined as the degree and duration of blood
flow loss, largely determines whether the brain suffers only
temporary dysfunction, irreversible injury to a few highly
neurons (Ischemic necrosis) or damage to extensive areas
involving all cell types (cerebral infarction)
• A failed delivery of oxygen and glucose to the brain
• Cerebral Infarction: irreversible cellular damage
• Cerebral Edema: Increases in the water content of the brain
(edema) accompany all types of ischemic and hemorrhagic
strokes
• Brain swelling and raised intracranial pressure.
42 Handbook of Neurological Physical Therapy
Contralateral hemiparesis
Sensory loss
Superior cerebellar artery Gait ataxia
Nausea
Dizziness
Headache
Progressing to ipsilateral hemiataxia
Dysarthria
Gaze paresis, Contralateral hemipa-
resis.
Laboratory Investigations
Hematology
• Complete blood count, glucose, prothrombin times, partial
thromboplastin time, lipid profile, electrolytes, creatinine, blood
Stroke Physical Therapy 43
Cardiovascular Tests
• 12 Lead (ECG) Electrocardiogram—to evaluate acute myocardial
ischemia and arrhythmias.
• Echocardiography—for cardiogenic source of emboli in acute
stroke.
• Stress Testing—to evaluate possible ischemic cardiovascular
disease.
Radiodiagnostic Imaging
CT Scan Imaging
• To identify other causes of focal neurologic dysfunction such as
neoplasms or subdural hematomas and to distinguish ischemic
from hemorrhagic stroke
• Can be used to evaluate CSF space, brain tissue perfusion.
Lumbar Puncture
• Diagnosing neurosyphilis or meningitis.
Cerebral Angiography
• Intracranial and extracranial cerebral angiography of elderly
patients to ischemic stroke
• Cerebral angiography should be reserved for specific indications
(e.g. for fibromuscular dysplasia, arterial dissection, and cranial
arteritis).
44 Handbook of Neurological Physical Therapy
Other Techniques
STROKE ASSESSMENT
• Observe for signs of increased intracranial pressure
• Assess level of consciousness and cognitive function
• Assess speech and communication
- Aphasia
- Perceptual deficits.
Stroke Physical Therapy
Assess Hearing
• Vision, check for homonymous hemianopsia.
Assess Coordination
• Finger to finger, heel to shin, supination , pronation test, finger to
nose, Romberg's sign .
Stroke Physical Therapy
Postural Control and Balance
• Using posturography, Berg Balance scale (0 -4).
Gait
• Circumduction gait or Hemiplegic gait,
• Equines gait,
• Unstable step lengths,
• Cadence,
• Insufficient pelvic rotation during swing,
• Weak hip flexors (external rotation with adduction, backward
leaning of trunk).
Assess ADLs
• Barthel Index, Functional mobility skills (FMS).
46 Handbook of Neurological Physical Therapy
Bobath
• Evaluation of motor patterns, qualitive assessment of movement
and postural patterns
• Based on three main recovery stage:
– Flaccidity stage
– Spasticity stage
– Stage of relative recovery.
Aims
Improve / Maintain Normal Oxygen and Ventilation
• Clearance of airways
• Improve chest expansion
Stroke Physical Therapy 47
A B
Figs 4.1A and B: Assisted Coughing
A B
• Removal of secretions
• Improve cough effectiveness (Fig. 4.1) Stroke Physical Therapy
• Improve breathing pattern/breathing sounds
• Prevent bed sores (Fig. 4.2).
A B
Figs 4.4 A and B: Stretching: (A) To right dorsiflexors of the ankle.
(B) Stretching right wrist flexors
Pulmonary Dysfunction/Care
Stroke Physical Therapy
Musculoskeletal Problems
• Passive ROM exercise should be started at the early stage of
stroke
• Use to prevent contractures, improving circulation and pre-
venting stiffness
• Avoid overstretching of soft tissue musculature and impingement
at glenohumeral joint, particularly in acute stage of stroke.
Stroke Physical Therapy 49
B
Figs 4.5 A and B: Positioning a critically ill patient may require several people
and continual monitoring of the patient's response
50 Handbook of Neurological Physical Therapy
Active Exercises
• Should be instituted as soon as the person is conscious (Carr.J,
2004)
• Active Assisted Arm exercise: Increase muscle tone and range of
motion (Figs 4.6 A to D).
A B
C D
Stroke Physical Therapy
Figs 4.6 A to D: (A) Active Assisted Arm Exercise (B) Patient is able to sit
independently (C) and (D) Active ROM exercise (Abduction)
Bobath/NDT Techniques
Brunnnstrom Method
Weight bearing exercise– to strengthen lower limb extensors.
Steeping exercise– to improve walking.
A B
C D
Figs 4.7 A to D:
52 Handbook of Neurological Physical Therapy
(E) (F)
E F
A B
C D
Figs 4.9 A to D: Post Stroke: Weakness of Hand muscles (A) and (B). He is
Difficult to hold and manipulate objects, i. e, wrist extension and forearm Supination
are absent. (C) and (D) Reaching is attempted. He attempts to reach the object in
paralysed or weak hand muscles
Exercise Conditioning
• Cycle Ergometry (Fig. 4.10)
• Walking
54 Handbook of Neurological Physical Therapy
EMG Biofeedback
• To improve motor functions
• Useful to strengthening Tibialis anterior, Quadriceps, Hams-
trings and upper extremity muscles
• EMG initiated electrical stimulation to improve arm and hand
functions in chronic hemiplegia (Kraft GH, et al 1992).
• Slow treadmill speeds (typically 0.01 -2.25 m/s) and light support
using an over head harness (typically 30% of body weight to
start) are used
• One or two Physical therapists provide manual assistance in
stabilization of trunk/pelvis and in movement of the paretic limb.
Isokinetic Training
• Use to increase strength and velocity control of movement.
Fig. 4.11: Ankle -Foot- Orthosis (AFO) Fig. 4.12: Wrist Cock up Splint
56 Handbook of Neurological Physical Therapy
Mobility Aids
• Wheel Chair: It is to promote early independence
• Walking aids: Quadripod cane, walker, Parallel bars, Cane or
stick (Fig. 4.13A and B) are frequently used for individuals with
poor balance and additional support through the lower limbs
during standing and walking.
Stroke Physical Therapy
A B
Complications of Stroke
• Immobility related complications are very common in the first
year in a severely disabling stroke. Patients who are more
frequently dependent at 3 months post stroke are likely to
experience a greater number of complications than those are less
dependent (Sackley C, et al. 2008). These complications include;
shoulder pain, shoulder hand syndrome, pressure sores,
contracture, deep vein thrombosis, shoulder pain
Stroke Physical Therapy 57
Investigations
• X-rays, MRI and Bone scan.
A B
Stroke Physical Therapy
C D
B
A
C
Figs 4.15A to C: Pressure sores: (A) Sacrum (B) Calcaneum (C) Occipital
Various stages
• Stage I – Non blanchable erythema of intact skin.
• Stage II – Partial Thickness skin loss.
• Stage III – Full thickness skin loss.
• Stage IV – Extension into muscles and bones.
Common Pressure Points
Lateral malleolus, Sacrum, Coccyx, Greater trochanter, calcaneum.
Occipital region.
60 Handbook of Neurological Physical Therapy
Prevention
• Avoid continuous pressure over bony prominences
• Changing the position once every two hours
• Avoiding friction and moisture over the skin
• Proper positioning of the limbs using sand bags.
Treatment
• Pressure relieving surfaces like water bed or alternating pressure
mattress
• Anterior, lateral, and press- up weight shifting techniques
• High protein diet supplemented with zinc and vitamins
• Wound debridement
• Antibiotics and Plastic surgery.
Contracture
Contracture was estimated as 30% or higher restriction when
compared with the good side, on physical examination by a Physical
therapist.
BIBLIOGRAPHY
• Anchlifee J. Strapping the shoulder in patients following a
Cerebrovascular Accident: A pilot study. Australian J Physiotherapy,
38(1), 37- 491.
• Anthony J, Zollo JR. Medical Secrets, Elsevier sciences, Philadelphia,
2006;475-98.
• Carr j, Shwpard R. Neuro Rehabilitation. 2nd ed Woburn MA,
Butterworth- Heineman 1998.
• Caillet R. The shoulder in Hemiplegia. FA Davis; Philadelphia, 1980.
• Chaudhuri JR, Taly TB. Neuro Rehabilitation: Concepts and Dynamics
in Neuro Rehabilitation; Principles and practice. Ahuja Book Company,
Bangalore, 2001; p. 38-48.
• Christopher MB, Catherine SM. Manual of Physical medicine and
Rehabilitation, Elsevier, Hanley and Belfus, Inc, 2002; 281-96.
• Dobkin BH. Stroke Rehabilitation, FA Davis, Philadelphia, 1996;157-
217.
• Dromerick A, Reding M. Medical and Neurological Complications
during inpatient Stroke Rehabilitation. Stroke, 1994;25: 358-61.
• Diane UJ, et al. Physical therapy interventions for patients with stroke
inpatient Rehabilitation facilities. APTA J; Jan 2005; 157-217.
• Dickstein R, Hocherman S, Pillar T, et al. Stroke Rehabilitation three
Exercise therapy Approaches, Phys Ther 1986;66:1233-38. Stroke Physical Therapy
• David OW, Valery LF, Robert DB. Hand Book of Stroke, 2nd ed,
Lippincott wiliams and wilkins 2006.
• Ernst E. A Review of Stroke Rehabilitation and Physiotherapy Stroke,
1990;21:1081-85.
• Evens RL, Hendricks Rd, Haselkorn JK, et al. The Family role in Stroke
Rehabilitation; A Review of the literature. Am J. Phys Med
Rehabilitation, 1992; 71:135-9.
• Edwards S. Neurological Physical therapy; A problem solving
Approach, London, Churchill Livingstone, 1996.
• Franceschini M, Carda S, Agosti M, et al. Walking after Stroke: What
does Treadmill Training with Body Weight Support Add to Overground
Gait Training in patients Early After Stroke? A Single Blind, randomized,
controlled trial, Stroke, 2009;40: 3079-85.
• Gibbons B. Stroke Rehabilitation, Nurs. Stand, 1994;8:49-54.
• Hesse S, Bertelt C, Jahnke MT, et al. Treadmill training with partial
weight support compared with Physiotherapy in nonambulatory
Hemiparetic patients stroke, 1995;26:976-81.
• Hidler H, Nicholes D, Pelliccio M, Brady K, Campbell DD, et al.
Multicenter randomized clinical trial evaluating the effectiveness of
62 Handbook of Neurological Physical Therapy
• Mant J, Carter J, Wade DT, et al. Family support for stroke; A rando-
mized controlled trial, Lancet, 2000; 356; 808-13.
• Nawoczenski D, Epler M. Orthosis in functional rehabilitation of the
lower limb. Philadelphia, WB Saunders Co.
• Nair, KPS, Taly AB. Stroke Rehabilitation; Traditional and Modern
Approaches. NeuroIndia, vol. 50, Dec 2002; PP; S85-S93.
• Stephen JM, Papadakis MA. Large current medical diagnosis and
treatment, 4th ed, Mc-Graw Hill, 2009.
• The Cochrane Database of syst. Review. Overground Physical therapy
Gait training for people with Chronic Stroke with mobility deficits.
Art, No: CD oo6075, 2009.
• Umphered D (ed) - Neurological Rehabilitation. 4th ed, St.Louis, CV
Mosby, 2004.
• Wild D. Stroke Focus, Stroke: A Nursing Rehabilitation role. Nurs.
Stand, 1994;8:36-9.
• Wade DT, et al. Physiotherapy intervention late after Stroke and
mobility, BMJ, 2009;13: 304-609.
C h ap ter
1234567890123456789012345678901212
1234567890123456789012345678901212
1234567890123456789012345678901212
CTION
ODUCTION
ODU
INTRODU
5
The human somatic cell is diploid with 46 chromosomes
(i.e. 23 pairs of chromosomes) of which 22 pairs are autosomes and
Physical Therapy
one pair of sex chromosome (XX in female and XY in male). The
germ cells or gametes are haploid cells (i.e. 23 chromosomes). During
in Muscular
fertilization the male and female gamete unite to form the zygote
(diploid).
The zygote formed undergoes mitosis repeatedly to form the
Dystrophy
embryo which later develops into an organism. Thus, all somatic
cells in a multicellular organism are descendants of one original
cell, the fertilized egg or zygote. Mitosis produces two daughter cells
per cycle and their genetic content is identical to mother cell.
Gametogenesis (formation of gametes) occurs only in specialized
cells (germ line) of the reproductive organs (gonads). In human, the
testes are male gonads and the ovaries are female gonads. Gamete
cells are produced through the process of mitosis. Mitosis consists
of two specialized, consecutive cell divisions in which the
chromosome number of resulting cells is reduced from a diploid
(2n) to a haploid (n) number. The number of chromosomes must be
reduced by half during gametogenesis in order to maintain the
chromosome number and characteristic of the species after
fertilization.
64 Handbook of Neurological Physical Therapy
MUSCULAR DYSTROPHY
CLASSIFICATION
• Duchenne type
• Becker
• Limb girdle (Erb)
• Facioscapulohumeral
• Emery-Dreifus
• Distal
• Ocular
• Oculopharyngeal
• Myotonic dystrophy.
Incidence
• The disease is inherited; males are likely to develop symptoms
than are women. Approximately one out of every 3,600 male
infants.
• Age at onset 1 to 5 years.
Pathology
• An absence of defect in the protein dystrophin (Xp21-2) which
results in progressive muscle degeneration leading to loss of
independent ambulation by the age of 13 years
Physical Therapy in Muscular Dystrophy 65
Clinical Manifestations
• Motor milestones delay
• Delayed walking
• Hypotonia
• Climbing stairs, rising from the ground after falling
• Positive Gower's sign – is always present, with boys needing to
turn on to their front and rise to standing from the floor using a
broad based stance, usually with the support of their hands on
their thighs (Figs 5.1A to F)
• Pelvic girdle muscle weakness
• Lordotic posture
• Trendelenburg gait or Waddling gait
• Weakness of musculature of the calf, Gluteal vastus lateralis,
Deltoid and Infraspinatus groups
• Tendon reflexes are diminished at the knees, biceps and triceps
• Contractures: Tendo-Achilles, Hamstrings, iliotibial band, Hip
A B
C D
Physical Therapy in Muscular Dystrophy
B D
Diagnosis
Laboratory Findings
• Serum Creatine kinase Level is elevated in Duchenne muscular
dystrophy. The usual serum concentration is 15,000 - 35,000 IU/
L (Normal < 160 IU/L)
• Electrocardiography (ECG), Echocardiography and Chest
roentgenogram - for assessment of heart
Physical Therapy in Muscular Dystrophy 67
Timed Tests
• Timed performance tests was used to measures of physical
performance (progressive weakness in children with DMD)
• Measure to walking speed , distance and to get up from the floor.
Aims
• To maintain physical function for as long as possible
• Prevent disabling consequences of secondary problems
Physical Therapy in Muscular Dystrophy
Passive Stretching
• Tendo-Achilles, Hamstrings, Iliotibial band, Iliopsoas, Later
shoulders, elbow, wrist muscles will need to stretched (Figs 5.2
and 5.3) and prevented for development of contractures.
Physical Therapy in Muscular Dystrophy 69
Resisted Exercise
• Should be prescribed as there is no evidence that they are useful
Physical Therapy in Muscular Dystrophy
but there are concerns that they may accelerate muscle damage.
Management
• Sitting AFOs are essential as painful contractures will develop,
that also impact negatively on posture
• Passive or active assisted exercise should be continued for
comfort, aesthetics and contracture prevention
• Pressure sores from sever contractures should be avoided
Aim
• Preventing further deformity
• Promoting better seating posture and comfort
• 90% of boys with Duchenne muscular dystrophy are likely to
develop a clinically significant scoliosis
• Provision of proper seating to prevent pelvic asymmetry and
provide postural support
72 Handbook of Neurological Physical Therapy
Problems
• Loss of respiratory muscle strength
• Ineffective cough and decreased ventilation
• Pneumonia
• Atelectasis and respiratory insufficiency.
Treatment
• Chest physical therapy
Physical Therapy in Muscular Dystrophy
• Breathing exercise
• Percussion of the chest
• Postural drainage
• Assisted coughing techniques
• Use of glossopharyngeal breathing (In essence forcing air into
the lungs using one's mouth)
• Spirometry
• Air stacking
• Mechanical assisted ventilation or mechanical assisted airway
clearance therapy.
Associated Problems
Bone Health
• Low bone mineral density even before loss of independent
ambulation. This may relate to their relative immobility even at
early stages of the disease
Physical Therapy in Muscular Dystrophy 73
BIBLIOGRAPHY
• Bakker JDJ, Groot I, Beckerman, Dejong, Lankhorst GJ. The effect of
knee ankle foot orthosis in the treatment of Duchenne muscular
dystrophy; review of the literature clinical rehab, 2000 April: (1), 14 (4):
p. 343-59.
• Cervellati S, Bettini N, Moscato M, Gusella A, dema E, Maresi R. Surgical
treatment of spinal deformities in Duchenne muscular dystrophy; A
long-term following study. Eur spine J, 2004;13 (5):441-8.
• Darry C, Vivo DE, Salvatore D. Herditary and Acquired types of
myopathy; Julia AM, Ralph DF, Catherine DD, Douglas JJ. Oski's
Pediatrics, Principles and Practice, Philadelphia, PA, USA, Lippincott
willams and Wilkins, 2006.
• Eckersley, PM. Elements of Pediatric Physiotherapy, Edinburgh, UK,
Churchill Livingstone, 1993;187-202
CTION
ODUCTION
ODU
INTRODU
6
The human somatic cell is diploid with 46 chromosomes
(i.e. 23 pairs of chromosomes) of which 22 pairs are autosomes and
Physical Therapy
one pair of sex chromosome (XX in female and XY in male). The
germ cells or gametes are haploid cells (i.e. 23 chromosomes). During
in Parkinson’s
fertilization the male and female gamete unite to form the zygote
(diploid).
The zygote formed undergoes mitosis repeatedly to form the
Disease
embryo which later develops into an organism. Thus, all somatic
cells in a multicellular organism are descendants of one original
cell, the fertilized egg or zygote. Mitosis produces two daughter cells
per cycle and their genetic content is identical to mother cell.
Gametogenesis (formation of gametes) occurs only in specialized
cells (germ line) of the reproductive organs (gonads). In human, the
testes are male gonads and the ovaries are female gonads. Gamete
cells are produced through the process of mitosis. Mitosis consists
of two specialized, consecutive cell divisions in which the
chromosome number of resulting cells is reduced from a diploid
(2n) to a haploid (n) number. The number of chromosomes must be
reduced by half during gametogenesis in order to maintain the
chromosome number and characteristic of the species after
fertilization.
76 Handbook of Neurological Physical Therapy
Incidence
• The incidence of PD is 18 per 100000 of population per year,
amounting to approximately 10000 new cases per year in the
UK. (Jones D and Playfer J 2004).
• PD is more likely to occur in males, because females survive
longer there is a fairly even distribution of overall cases between
the sexes.
• Affects 0.3% of total population (1% of population older than 55
Physical Therapy in Parkinson’s Disease
years).
Etiology
• Aging is not cause of parkinson‘s disease
• Toxin exposure
• Genetic predisposition and oxidative stress.
Pathophysiology
• Dopamine depletion due to degeneration of the dopaminergic
nigrostriatal system leads to an imbalance of dopamine and
acetylcholine, which are neurotransmitters normally present in
the corpus striatum.
Clinical Manifestations
Cardinal Features
• Resting tremor
Physical Therapy in Parkinson’s Disease 77
• Rigidity
• Bradykinesia
• Postural instability.
Resting Tremor
• It is most common presenting feature
• Resting tremor of 4 to 6 cycles per second is most conspicuous at
rest
• Although it may ultimately be present in all limbs.
Rigidity
• Rigidity is an increase resistance to passive movement
• Parkinson’s rigidity is characterized by an increased resistance
to passive movement through out the entire range of motion, in
both agonist and antagonist muscle power
• Functional outcomes: Flexed posture, lack of trunk rotation,
reduced joint range of movement during postural transitions
and gait.
Postural Instability
• It is a common and serious problem in parkinson’s disease. Up
to 90% of all parkinson's patient to diminished in postural
reactions
• Thirty eight of hundred patients with PD fall 13% experience
fractures, 18% hospitatalization and 3% are confined wheelchair.
• Impairment of swallowing
• Impairment of fine or rapidly alternating movements and
micrographia
• Shuffling gait
• Unsteadiness on turning
• Difficult in stopping and a tendency to fall
• Sleep disturbance
• Urinary dysfunction
• Visual disturbances.
Psychiatric Symptoms
• Depression and dementia
Diagnosis
• Clinical Examination: It is based on presence of bradykinesia,
muscular rigidity, resting tremor, and postural instability
• Magnetic Resonance Imaging (MRI) scans: Are normal, with
variable amounts of atrophy
• Single photon emission computed tomography (SPECT): May
shows decrease in dopamine transporters
Physical Therapy in Parkinson’s Disease
CLASSIFICATION OF DISABILITY
Modified Hoehn and Yahr Score (1967) (Table 6.1)
Stage Description
0 No signs of disease
1 Unilateral disease
1.5 Unilateral plus axial movement
2 Bilateral disease, without impairment of balance
2.5 Mild bilateral disease; recovery on pull test
3 Mild to moderate bilateral disease; some postural instability;
capacity for living independence
4 Severe disability; still able to walk or stand unassisted.
5 Wheelchair bound or bedridden unless aided.
Physical Therapy in Parkinson’s Disease 79
ASSESSMENT
• Patient History
• Assess cognitive and behavioral status:
– Intellectual impairment
– Dementia
– Check for memory status deficits
– Bradphrenia (Slowing of thought processes)
– Depression
• Assess communication:
– Dysarthria
– Hypophonia are common
– Mask-like face with frequent blinking and expression, writing
becomes slow
• Assess for oromotor and nutritional status:
– Dysphagia is common problem (Chewing and swallowing).
• Assess respiratory status:
– Breathing pattern, vital capacity, decreased chest expansion.
• Assess vision:
– Check for blurring, cog wheeling eye pursuit
Cueing Strategies
• In Patient with Parkinson's disease, gait is improved by applying
visual or auditory cues, which have trained during active gait
training
• Cues are stimuli from environment or generated by the patient,
which the patient uses, consciously or not , to facilitate (automatic
or repetitive) movements. It is not clear exactly how cues improve
movement
• Perhaps they provide external rhythm that can compensate for
the improperly supplied internal rhythm of the basal ganglia,
82 Handbook of Neurological Physical Therapy
Balance
• Balance training (where patients are taught to use visual and
vestibular feedback)
• Combined with lower extremity strength training is effective in
improving balance in patients with PD.
Physical Activity
• The exercise program aim is to improve range of motion combined
with activity related to (e.g. gait or balance exercise)
• Improves ADL functioning
• Strength training program increasing muscle power ( strengthen
low back and hip extensors)
• Range of motion trunk exercises
Physical Therapy in Parkinson’s Disease 83
BIBLIOGRAPHY
• Bergen JL, Toole T, Elliot RG, Wallace B, Robinson K, Maitland CG.
Aerobic exercise intervention improves aerobic capacity and
Movement initiation in Parkinson’s disease patients. Neuro Rehab,
2002; 17:161-8.
• Bridgewater KJ, Sharpe M - Trunk muscle training and early
Parkinson disease. Phys Ther; 1997; vol 13: 139-53.
• Brusse KJ, Zimdars S, Zaleski KR, Steffen TM. Testing Functional
performance in people with Parkinson’s disease. Phys Ther, 2005;
vol 85(2): 134-41.
• Comella CL, Stebbins GT, Brown TN, Goetz CG. Physical therapy
and Parkinson’s disease; A Controlled Clinical trial. Neurology, 1994;
44(1); 376-78.
CTION
ODUCTION
ODU
INTRODU
7
The human somatic cell is diploid with 46 chromosomes
(i.e. 23 pairs of chromosomes) of which 22 pairs are autosomes and
Spinal Cord Injury
one pair of sex chromosome (XX in female and XY in male). The
germ cells or gametes are haploid cells (i.e. 23 chromosomes). During
Rehabilitation
fertilization the male and female gamete unite to form the zygote
(diploid).
The zygote formed undergoes mitosis repeatedly to form the
embryo which later develops into an organism. Thus, all somatic
cells in a multicellular organism are descendants of one original
cell, the fertilized egg or zygote. Mitosis produces two daughter cells
per cycle and their genetic content is identical to mother cell.
Gametogenesis (formation of gametes) occurs only in specialized
cells (germ line) of the reproductive organs (gonads). In human, the
testes are male gonads and the ovaries are female gonads. Gamete
cells are produced through the process of mitosis. Mitosis consists
of two specialized, consecutive cell divisions in which the
chromosome number of resulting cells is reduced from a diploid
(2n) to a haploid (n) number. The number of chromosomes must be
reduced by half during gametogenesis in order to maintain the
chromosome number and characteristic of the species after
fertilization.
86 Handbook of Neurological Physical Therapy
Incidence
• An annual incidence of 15 to 40 traumatic SCI cases per million
populations has been reported worldwide, and a conservative
estimate for India would be 20,000 cases are added every year
• Sixty to seventy percent of them are illiterate, poor villagers
• In Asia pacific region, Australia with 2003 population of 20
million reported an incidence of 300-400 new cases per year or
15 to 20 per million, and a prevalence of 10,000 persons with
Spinal cord injury.
Spinal Cord Injury Rehabilitation
Mode of Injury
• The most common cause of injury was fall from height including
roof, trees, electricity pole, and motor vehicle accidents
• Falls were more prominent in second and third decades. Road
side accidents were commoner in third and fourth decade.
Brown-Sequard Syndrome
• Hemisection of spinal cord due to trauma, tumor
• Ipsilateral paralysis and loss of proprioception due to the
crossing of the corticospinal tracts and dorsal columns in the
brainstem
• Produces contralateral loss of pain and temperature sensation
due to local crossing of spinothalamic tracts in the spinal cord.
Sacral Sparing
• Sparing of tracts to sacral segments, with preservation of perianal
sensation, rectal sphincter tone and active toe flexion.
88 Handbook of Neurological Physical Therapy
Paraplegia
• Impairment or loss of motor, sensory and or autonomic function
in thoracic, lumbar or sacral segments of the spinal cord
• Injury occurs between T1 and T12, involves both lower extremities
and trunk.
Spinal Cord Injury Rehabilitation
Heterotopic Ossification
• Heterotopic ossification is defined as the formation of new
osseous material in tissues where bone formation does not
usually occur
• Ossification of soft tissues near and around joint regions occurs
most commonly after spinal cord injury, traumatic injuries, burns,
general trauma, total joint surgeries and occasionally in pediatric
amputation patients
90 Handbook of Neurological Physical Therapy
Spasticity
• Spasticity secondary to SCI and other CNC injury damage is
common
• Spasticity developed in 67% of SCI patients by discharge (of first
injury-related hospitalization (Timothy LS, 2009)
• It is more prevalent in cervical and high thoracic injuries than in
lower thoracic or Lumbosacral injuries
• Clinical manifestations of hypertonicity (increased muscle tone),
clonus (a series of rapid muscle contractions), spastic paralysis,
hyperreflexia (exaggerated deep tendon reflexes), Babinski’s sign
and clasp-knife rigidity
• Assessment: On Physical examination, spasticity can be assessed
using the Ashworth scales (original and modified), spasm scale
(Table 7.2), and physicians rating scale
• The Ashworth scale (or modified Ashworth scale) measuring
rigidity on a 1-5 basis and the spasm scale, quantifying number
of spasms per hour (Table 7.1).
Spinal Cord Injury Rehabilitation
Table 7.1: Ashworth and Spasm scale
ASHWORTH SCALE
1 No increase in tone
2 Slight increase in tone , giving a "catch" when affected part
moved in flexion or Extension.
3 More marked increase in tone, but affected part easily flexed.
4 Considerable increase in tone; passive movement difficult.
5 Affected part rigid in flexion or extension
Score Criteria
0 None
1 No spontaneous spasms, vigorous sensory and motor
stimulation results in spasms
2 Occasional spontaneous and easily induced spasms
3 More than 1 but < 10 spontaneous spasms per hour
4 > 10 spontaneous spasms per hour.
Treatment
• The best management is prevention in the first few months after
injury ( Bernes et al, 2001)
• Physical therapy is usually necessary in every spastic patient
Spinal Cord Injury Rehabilitation
ASSESSMENT
Respiratory System
• Assess for Oxygen saturation level
• All respiratory muscles, abdominal muscles
• Auscultation
• Coughing.
Spinal Cord Injury Rehabilitation 93
Cardiovascular System
• Pulse
• Blood pressure
• Heart sounds.
Gastrointestinal Tract
• Abdomen, bowel sounds normal/abnormal.
Urinary Tract
• Voluntary bladder control
• Indwelling catheter was inserted on admission.
Sensory Examination
Examination for Sensations Tests was Performed
• Touch, pain, joint position, deep pressure
• Record level of normal sensation by drawing a line on the patients
skin.
Motor Examination
• The Royal Medical Research Council of Great Britain scale can
be based to assess power (Table 7.2)
• Abdominal and erector spinae muscle group could not be tested Spinal Cord Injury Rehabilitation
according to this scale and only a subjective grading based on
palpation was done
Grade Description
REFLEXES
• Deep tendon reflexes (DTR): Biceps, triceps, patellar, ankle jerk.
• Superficial reflexes: Abdominal (Upper, Lower) reflex,
cremasteric, bulbocavernosus reflex.
• Grading: 0- 4
Investigations
Plain X-rays
• Cervical spine X-ray: from craniocervical junction to C7/T1
Spinal Cord Injury Rehabilitation
Occupational Therapy
• Transfer to the bed and the toilet
• Endurance training by pushing his/her wheelchair
• Basic wheelchair manipulation
• Balance in sitting
• Handling in wheelchair
• Back wheel balance
• Education.
Spinal Cord Injury Rehabilitation 97
Spinal Orthosis
Cervical Orthosis
• Aim: Control pain, protect further injury, limit or restrict
movement, support soft tissues, control cervical spine position.
T6-T12 Level
• Caliper walker with rollator and crutches.
L3 level
• Appropriate orthosis or walking aid
98 Handbook of Neurological Physical Therapy
Ambulatory Aids
• Canadian type of elbow crutches
• Walking frames
• Wheelchair.
Robotic Devices
• Robotic device use of automated driven gait orthosis ambulation
training has been proposed to significantly, reduce the load on
therapists during ambulation training.
Pain Management
• Electrothermotherapy, positioning, TENS, movement re-
education and acupuncture.
BIBLIOGRAPHY
• American Spinal injury Association: International standards for
neurological classification of spinal cord injury. Revised; Chicago;
American Spinal injury Association, 2000.
• Brammmer CM, Catherine Spires, M. Manual of Physical medicine
and rehabilitation. Elsevier, 2002; p. 119-38.
• Field Fote EC. Spinal cord control movement: Implications for
locomotor rehabilitation following spinal cord Injury. Phys Ther, 2000;
80(5): 477-84.
• Gourassini MA, Noton JA, Ducherer JN, Roy FD, Yang JF. Changes in
locomotor muscle activity after treadmill training in subjects with in
complete spinal cord injury. J Neuro Physiol, 2009;101(2):969-79.
• Kathleen A, Curtis, Karry lMH. Spinal cord injury community follow
up: Role of physical therapist; Phys Ther, 1986; 66(9): 1370-5.
• Katz RT, Spasticity, In: O' Young B, Young MA, steins SA. PM and R
secrets, Phildelphia; Hanley and Belfus, 1997; p 487.
• Mangold S, Keller T, Curt A, Diet V. Transcutaneous functional electrical
stimulation for grasping in subjects with cervical spinal cord injury. Spinal Cord Injury Rehabilitation
Spinal cord, 2005;43: 1-13.
• National institute of Neurological Disorders and Stroke (National
institute of Health) http//www.ninds.gov/disorders/spasticity/
spasticity/htm, accessed june 21, 2009.
• Pollack SF, Axen K, Spietholz N, Levin N, Haas F, Ragnarsson KT.
Aerobic training effects of electrically induced lower extremity exercise
in spinal cord injured people. Arch Phys Med Rehabili, 1969; 70;(3):
214-5.
• Peter AC, Lim, Adela MT. Recovery and regeneration after spinal
cord injury: A review and summery of recent literature. Ann Acad
med Singapore, 2007; 36:49-57.
• Riva G, Italiano IA. Virtual reality in paraplegia; A test bed application.
The International J. Virtual Reality, 2001; 5(1): 1-10.
• Shehu BB, Ismail NJ. Continuing education: Practical management of
spinal cord injury, annals African medicine; 2004; 3(1): 46-52.
100 Handbook of Neurological Physical Therapy
• Staas WE, Formal CS, Freedman MK, et al. Spinal cord injury and
Spinal cord injury Medicine. In DeLisa JA (ed): Rehabilitation Medicine,
Principles and Practice, 3rd ed, Philadelphia, Lippincott Willams and
Wilkins, 1998, p. 1276-7.
• Timothy L, Sternberg. Treatment of Spasticity associated with spinal
cord injury and other central nervous system damage. North East
Flordia Medicine, 2009; 60(3): p. 19-22.
• Wening A, Mullers S. Laufband. Locomotion with body weight support
improved walking in persons with severe spinal cord injuries,
Paraplegia, 1992; 30: 229-38.
• Yen HL, Chua K, Chan W. Spinal cord Injury rehabilitation in singapore.
Int J Rehabili Res 1998;21: 375-87.
Spinal Cord Injury Rehabilitation
C h ap ter
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CTION
ODUCTION
ODU
INTRODU
8
The human somatic cell is diploid with 46 chromosomes
(i.e. 23 pairs of chromosomes) of which 22 pairs are autosomes and
Physical Therapy
one pair of sex chromosome (XX in female and XY in male). The
germ cells or gametes are haploid cells (i.e. 23 chromosomes). During
in Cerebral Palsy
fertilization the male and female gamete unite to form the zygote
(diploid).
The zygote formed undergoes mitosis repeatedly to form the
embryo which later develops into an organism. Thus, all somatic
cells in a multicellular organism are descendants of one original
cell, the fertilized egg or zygote. Mitosis produces two daughter cells
per cycle and their genetic content is identical to mother cell.
Gametogenesis (formation of gametes) occurs only in specialized
cells (germ line) of the reproductive organs (gonads). In human, the
testes are male gonads and the ovaries are female gonads. Gamete
cells are produced through the process of mitosis. Mitosis consists
of two specialized, consecutive cell divisions in which the
chromosome number of resulting cells is reduced from a diploid
(2n) to a haploid (n) number. The number of chromosomes must be
reduced by half during gametogenesis in order to maintain the
chromosome number and characteristic of the species after
fertilization.
102 Handbook of Neurological Physical Therapy
Incidence
• The incidence of CP per 1000 births by birth weight is 90 among
infants weight less than 1500 g
• Due to increased survival of premature infants with low birth
weight.
Contd...
Prenatal Perinatal Postnatal
Teratogenic mental Abnormal Coagulopathies
retardation presentations
Maternal seizures Trauma
Maternal Infection
hyperthyroidism
Placental Bradycardia and hypoxia
complications
Additional trauma Seizures
Multiple gestation Hyperbilirubinemia.
CLINICAL MANIFESTATIONS
Spastic Diplegic Cerebral Palsy (Little Disease)
• It is most common type of cerebral palsy (80% of cases) Physical Therapy in Cerebral Palsy
• Lesions motor cortex
• Eighty percent cases are diplegic child
A B
104 Handbook of Neurological Physical Therapy
Diagnosis
MRI Scan of Brain: To determine location and extent of structural
lesions or associated congenital malformations.
CT Scan: Useful for detecting calcifications associated with
congenital infections.
AIM
• Improve muscle strength
• Improve local muscular endurance
• Maintain or improve joint range of motion
• Decrease and prevent joint contractures
• Improve balance
• Postural control
• Mobility and ability to transfer (for instance from bed to
wheelchair).
• Gait
• ADLs.
Physical Therapy in Cerebral Palsy
Treatment /Techniques
Passive range of motion (PROM) and Active range of
motion (AROM) exercise (Figs 8.4 to 8.6)
• Repetitive PROM exercise to improve and maintain joint mobility.
Fig. 8.6: AROM exercise in Fig. 8.7: Posture correction and weight
shoulder flexion bearing of the both lower extremity
Basic Principle
• The motor abnormalities in children with cerebral palsy are due
to failure of normal development of postural control and reflexes
because of the underlying dysfunction of the central nervous
system (Butler C, 2001).
Aim
• To facilitate normal motor development and function and to
Physical Therapy in Cerebral Palsy
Patterning
• The concept of patterning is based on theories developed by Fay,
Delacto and, in the 1950 and 1960
Physical Therapy in Cerebral Palsy 113
Hippotherapy (HT)
• To improve muscle tone, balance and postural control.
Acupuncture
• To reduce painful muscle spasms and overall motor function
(Shi B, Bu H and Lin L, 1992).
Vojta Method
• The persistence of these newborn reflex patterns in a child with
cerebral palsy interferes with postural development
• Facilitating the development of reflex locomotion.
114 Handbook of Neurological Physical Therapy
BIBLIOGRAPHY
• Butler C, Darrah J. Effects of neuro developmental treatment (NDT)
for cerebral palsy: an AACPDM evidence report. Dev Med Child
Neurol; 2001;43:778-90.
• Dali C, Hansen FJ, Pedersen SA, et al. Threshold electrical stimulation
in ambulant children with cerebral palsy: a randomized double-based
placbocontrolled clinical trial. Dev Med Child Neuro; 2002;44:364-69.
• Dilip R Patel. Therapeutic Interventions in cerebral palsy; symposium
on Developmental and behavioral disorders II. Indian J Pediatric, 2005;
72(11): 979-89.
• Koman LA, Smith BP, Shilt JS. Cerebral palsy. Lancet, 2004;363:1619-
31.
• Kliegman, Behrman, Jenson, Stanton. Nelson Text Book of Pediatrics;
Cerebral palsy, 18th ed, Elsevier, 2008; 2: 2494-8, 670.
• Kliegman, Greenbanm Lye. Practical strategies in Pediatric Diagnosis
and Therapy. 2nd ed, Elsevier, Philadelphia, 2004; p. 651.
• Kerr C, Mc Dowell B, McDonough S. Electrical stimulation in cerebral
palsy; a review of effects on strength and motor function. Dev Med
Child Neurol, 2004;46:205-13.
• Mayston M. Physical Therapy management of cerebral palsy; an update
on treatment approaches, clinics in developmental medicine; 2004;
161:147-60.
• Meregillano G. Hippotherapy. Phys Med Rehabil clin N Am 2004;
15(14):843 -54.
Physical Therapy in Cerebral Palsy
CTION
ODUCTION
ODU
INTRODU
9
The human somatic cell is diploid with 46 chromosomes
(i.e. 23 pairs of chromosomes) of which 22 pairs are autosomes and
Physical Therapy
one pair of sex chromosome (XX in female and XY in male). The
germ cells or gametes are haploid cells (i.e. 23 chromosomes). During
in Cerebellar
fertilization the male and female gamete unite to form the zygote
(diploid).
The zygote formed undergoes mitosis repeatedly to form the
Ataxia
embryo which later develops into an organism. Thus, all somatic
cells in a multicellular organism are descendants of one original
cell, the fertilized egg or zygote. Mitosis produces two daughter cells
per cycle and their genetic content is identical to mother cell.
Gametogenesis (formation of gametes) occurs only in specialized
cells (germ line) of the reproductive organs (gonads). In human, the
testes are male gonads and the ovaries are female gonads. Gamete
cells are produced through the process of mitosis. Mitosis consists
of two specialized, consecutive cell divisions in which the
chromosome number of resulting cells is reduced from a diploid
(2n) to a haploid (n) number. The number of chromosomes must be
reduced by half during gametogenesis in order to maintain the
chromosome number and characteristic of the species after
fertilization.
116 Handbook of Neurological Physical Therapy
CEREBELLAR ATAXIA
• Cerebellar ataxia is a result of damage to the cerebellum or parts
of the brain that connect to the cerebellum. This includes cerebellar
peduncles and the pons, and red nucleus
• Cerebellar ataxia refers to a condition of unsteadiness of gait.
Ataxia can result of damage to the cerebellum ( cerebellar ataxia)
or posterior columns of the spinal cord (sensory ataxia) or
dysfunction of the vestibular system ( vestibular ataxia).
Epidemiology
• Estimated prevalence: One in 12,500 adults with autosomal
dominant cerebellar ataxia in the north east England
• Estimated minimum prevalence 10.2 in 100,000 people with late
onset of cerebellar ataxia in south wales.
Etiology
• Vascular
• Traumatic
• Developmental
Physical Therapy in Cerebellar Ataxia
• Neoplastic/Paraneoplastic
• Infections
• Inflammatory (e.g. Multiple sclerosis)
• Metabolic
• Toxic/drug-related (e.g. Alcohol)
• Epilepsy (In children).
Clinical Manifestations
• Incoordination and unsteadiness (Figs 9.2A and B)
• Clumsiness
• Nystagmus
• Ataxia gait and in extreme cases impaired sitting balance (Fig. 9.1)
• Intention tremor
• Dysmetria or past-pointing – difficulty in controlling the
termination of movements
• Dysdiadochokinesis – difficulty performing rapid alternating
movements
Physical Therapy in Cerebellar Ataxia 117
A B
Diagnostic Investigations
• Creatinine, liver enzymes, electrophoresis, ESR, CRP, TFT,
Vitamin B12, fiolate, cholestrol, FBC.
• MRI of the brain
• Lumbar puncture
• Genetic tests
• EMG
• EEG.
Assessment
• The assessment of ataxia should be integrated into a functional
analysis were:
Heel-to-shin Test
• Patient is supine lying, and to place the heel of one leg on to the
shin of the other, near the knee, then to slide the heel down the
shin towards the foot
• Difficulty placing the heel because the dysmetric component of
dysfunction.
Romberg Test
• The test is performed in standing position. Patient is asked to
stand still with arms stretched forward at shoulder height, with
eyes open then closed
• Test for measuring ataxia
• Romberg sign can be using a force plate to measure of foot
pressure (Black, et al. 1982).
Physical Therapy in Cerebellar Ataxia 119
• PNF
• Frenkel's exercise
• Dynamic training of postural with task and activity focus
• Gait and balance training
• Strengthening exercises
• Flexibility
• Visually guided movements (finger-to- nose test)
• Manipulation of visual information and hand movements
• Cold therapy–to decrease in muscle spindle, reduction in
response of the long latency tone stretch reflex, decrease in nerve
conduction velocity
• Wrist weighting–to reduce upper limb tremor
• Fitness training
• Mobility aids–light touch as a balance aid may be helpful for
postural orientation and stability.
Physical Therapy in Cerebellar Ataxia 121
OCCUPATIONAL THERAPY
• Occupational therapy is important intervention for patients with
progressive neurological conditions in neurological conditions
in maintaining independence and quality of life and to enable
people to participate in self care
• Conservation energy technique
• Self care and toileting– encourage to bath or shower and consider
providing seating with support for the back and arms
• Use thermoregulation devices on taps
• Bed, chair and toilet transfers
• Indoor mobility–use of walking aids in the home and other
environments
• Use of walking frames may need to be reconsidered in very small
areas
• Falls prevention.
BIBLIOGRAPHY
• Ataxia UK. Management of the Ataxias towards Best Clinical Practice,
2009.
• Fuller G. Neurological Examination Made Easy. 3rd ed, Churchill
Livingstone, 2005.
• Gill B. et al. Rehabilitation of balance in two patients with cerebellar
dysfunction, Phys Ther, 1999;77(5): 534-52.
• Gillen G. Improving mobility and community access in an adult with
ataxia; A Case study. Am J Occup Ther, 2002;56:462-6.
• IIg.W, Syonfzik M, Brotz D, Burkand S, Giese MA, Scholes L. Intensive
coordinate training improves motor performances in degenerative
cerebellar disease.
• Jeka JJ. Light touch contact as a balance aid, Phys Ther, 1997; 77(5): 476-
87.
122 Handbook of Neurological Physical Therapy
CTION
ODUCTION
ODU
INTRODU
10
The human somatic cell is diploid with 46 chromosomes
(i.e. 23 pairs of chromosomes) of which 22 pairs are autosomes and
Orthotics in
one pair of sex chromosome (XX in female and XY in male). The
germ cells or gametes are haploid cells (i.e. 23 chromosomes). During
Neurorehabilitation
fertilization the male and female gamete unite to form the zygote
(diploid).
The zygote formed undergoes mitosis repeatedly to form the
embryo which later develops into an organism. Thus, all somatic
cells in a multicellular organism are descendants of one original
cell, the fertilized egg or zygote. Mitosis produces two daughter cells
per cycle and their genetic content is identical to mother cell.
Gametogenesis (formation of gametes) occurs only in specialized
cells (germ line) of the reproductive organs (gonads). In human, the
testes are male gonads and the ovaries are female gonads. Gamete
cells are produced through the process of mitosis. Mitosis consists
of two specialized, consecutive cell divisions in which the
chromosome number of resulting cells is reduced from a diploid
(2n) to a haploid (n) number. The number of chromosomes must be
reduced by half during gametogenesis in order to maintain the
chromosome number and characteristic of the species after
fertilization.
124 Handbook of Neurological Physical Therapy
ORTHOTICS
• Orthotics is a passive external device that support loads or assist
or restrict relative motion between body segments. The word
orthotics is derived from Greek for making or setting straight,
and is a general term that encompasses bracing and splints.
Orthotics or Orthoses plays an important role in the rehabilitation
of patients with motor impairments. Orthotics include devices
for the neck, upper limb, trunk and lower limb that are designed
to guide motion, bear weight align body structures, protect joints
or correct deformities. Orthoses are designed to work in
cooperation with the intact body, and either control or assist
movement. (Selzer, Clarke et al, 2003)
Trunk Orthosis
Scott-Craig Orthosis
• A metal knee ankle foot orthosis (KAFO) used by spinal cord
Orthotics in Neurorehabilitation
injury patients.
Halo Orthosis
• An external brace designed to stabilize the cervical vertebrae.
Four-Poster Orthosis
• Two plates (occipital and thoracic) with two anterior and two
posterior posts to stabilize the head
• Used for moderate levels of control in individual with cervical
fracture/spinal cord injury.
Jewett Orthosis
• An external method of providing stabilization to the thoracic
and lumbar vertebrae
126 Handbook of Neurological Physical Therapy
• Prevents hyperextension
• Three points of pressure on the sternum, lumbar spine and
symphysis pubis.
Knight-Taylor Brace
• A method of applying external stabilization to the thoracic and
lumbar vertebrae
• Typically utilized for fractures above the L3- region.
Hand Orthoses
• To provide elastic resistance to finger extension, thus enhancing
a strengthening program following stroke.
BIBLIOGRAPHY
• Biering SF, Ryde H, Bojscn MF, Lyquist E. Shock absorbing material
on the shoes of long leg braces for paraplegic walking. Prosthet orthot
Int., 1990;14:27-32.
• Braddom RL. Physcial Medicine and Rehabilitation, 3rd ed. Philadelphia,
WB. Saunders, 2007; p. 325-42.
• Cusick B, Sussman MD. Short Leg Casts; their role in the management
of Cerebral palsy. Physcial and Occupational Ther in pediatric, 1982;
2:93-110.
• Fess EE. Hand and upper extremity Splinting: Principles and Methods,
Orthotics in Neurorehabilitation
Orthotics in Neurorehabilitation
49.
• Tan T. Practical Manual of P Mand R. St. Louis, Mosby, 1998.
• Redford JB. Orthotics: Clinical Practice and Rehabilitation technology,
New york, Churchill Livingstone, 1995; p 103-19.
• Redford JS, Patel AT. Orthotic Devices in the management of Spinal
Disorders, Phys Med rehabil State Art Rev, 1995;9:709-24.
ODU
INTRODU CTION
ODUCTION
The human somatic cell is diploid with 46 chromosomes
Appendices
(i.e. 23 pairs of chromosomes) of which 22 pairs are autosomes and
one pair of sex chromosome (XX in female and XY in male). The
germ cells or gametes are haploid cells (i.e. 23 chromosomes). During
fertilization the male and female gamete unite to form the zygote
(diploid).
The zygote formed undergoes mitosis repeatedly to form the
embryo which later develops into an organism. Thus, all somatic
cells in a multicellular organism are descendants of one original
cell, the fertilized egg or zygote. Mitosis produces two daughter cells
per cycle and their genetic content is identical to mother cell.
Gametogenesis (formation of gametes) occurs only in specialized
cells (germ line) of the reproductive organs (gonads). In human, the
testes are male gonads and the ovaries are female gonads. Gamete
cells are produced through the process of mitosis. Mitosis consists
of two specialized, consecutive cell divisions in which the
chromosome number of resulting cells is reduced from a diploid
(2n) to a haploid (n) number. The number of chromosomes must be
reduced by half during gametogenesis in order to maintain the
chromosome number and characteristic of the species after
fertilization.
132 Handbook of Neurological Physical Therapy
APPENDIX : A
Domain Score
Eyes opening
Open spontaneously 4
Open verbal command 3
Open to pain 2
No response 1
APPENDIX: B
CLINICAL SYNDROMES
• Central cord
• Brown-Sequard
• Anterior cord
• Conus Medullaris
• Cauda Equina.
Ref.: Lin.V (2003) – Spinal Cord Injury Medicine: Principle and Practice,
Appendices
New York.
134 Handbook of Neurological Physical Therapy
APPENDIX: C
Score Description
0 No symptoms.
1 No significant disability despite symptoms; able to carry out all
duties and activities.
2 Slight disability; unable to carry out all previous activities but
able to look after own affairs without assistance.
3 Moderate severe disability requiring some help but able to walk
without assistance.
4 Moderate severe disability; unable to walk without assistance
and unable to attend to own bodily needs without assistance.
5 Severe disability; bedridden, incontinent, and requiring constant
nursing care and attention.
APPENDIX: D
Level Response
I No response: Patient does not respond to external stimuli and
appears asleep.
II Generalized response: Patient reacts to external stimuli in non-
specific, inconsistent
– And non purposeful manner with stereotypic and limited
response.
III Localized response: Patient response specifically and consis-
tently with delays to stimuli but may follow simple commands for
motor action.
IV Confused, inappropriate, agitated response: Patients exhibits
bizarre, non purposeful,
– Incoherent, or inappropriate behaviors; has no short-term
recall; attention is short and
– Nonselective.
V Confused, inappropriate, nonagitated response. Patient gives
random, fragmented, and non purposeful responses to complex
or unstructured stimuli. Simple commands are:
– Followed consistently, memory and selective attention are
impaired and new information
Is not retained.
VI. Confused, appropriate response: Patient gives context-
appropriate, Goal directed
– Responses, dependent on external input for direction. There
Appendices
APPENDIX: E
Grade Description
A Attension tests 5
Autonomic dysreflexia 89
Activities of daily livings (ADLs) 82 Bladder, bowel dysfunction 90
Spinal cord injury 86 Spinal cord injury- related. 86
ADLs 82, 106
Evaluation scales 45 B
Adductors innervations of 11
Airway clearances 46 Balance 81, 82
American spinal cord injury asso- Babinski sign 17
ciation (ASIA) 88, 133 Basilar artery 42
Scale Baclofen
Angiography 25, 43 As spasticity treatment 92
Cerebral for stroke evaluation 43 cerebral palsy 102
Acupuncture 113 Intrathecal pump 92
Ankle clonus 105 Barthel's Index 45
Contracture 104 Basilar artery 42
Deformity of ankle Beds, pressure ulcer prevention 62
foot orthosis 55, 98 Behavior disturbance 4
Anterior cord syndrome 87 Bell’s Palsy 30
Aphasia 5 Biceps reflex 15
Stroke related to 44 Biofeedback 35
Ashworth scales Bladder dysfunction 90
For spasticity management 91 Urinary incontinence 93
Asymmetric tonic neck reflex 18 Hyperreflexia 15
Parkinson's related 76
Ataxia
Spinal cord injury related 86
Cerebellar lesions 116
Blood flow 40
Friedreich's 120
Blood pressure
dysarthria 117
See also hypertension, hypo-
dysdiadochokinesia 116
tension 8
Dementia 79
Bobath approach 46, 108
hypotonia 12, 117
Bowel dysfunctions 90
Nystagmus 116 Brachialis muscle innervations 15
Tremor 77 Bradycardia 91
Athetoid 105 Brown-Sequard syndrome 87
Cerebral palsy related 103 Brunnstrom 51
138 Handbook of Neurological Physical Therapy
C Dementia 79
stroke 40
Cane 56 Parkinson disease 76
Carotid artery 42 Depression 79
Cardiorespiratory Developmental delay 102
dysfunction 48 Diplegia 103
Casts, splints management 55 Diplopia 117
Cerebral arteries 42 Disability scale 78
Vascular supply and Dressing for pressure sores 60
distribution 41 Dynamometer 9
Dysdiadochokinesia 21
Cerebrovascular syndrome 42
Dysmetria 116
Cerebral hemispheres 40
Dysphagia 79
Cerebral palsy 102
Oropharyngeal 121
Extrapyramidal 105 Parkinson's disease 76
Pyramidal 103 Stroke 40
Cerebrovascular accidents see also Pneumonia risk factors 46
stroke 40
Chorea 14 E
cerebral palsy related 102
choreoathetoid movements 105 Electrical stimulation 35, 112
Coma scale 3, 132 Elecrtomyography 26, 67
Computed tomography (CT) 24 see Muscular dystrophy 64
Head for stroke 43 Feed back 54
Conductive Education 112 Bell's palsy 30
Stroke 40
Contractures 56, 60
Edema 41
Constraint- induced therapy 55
Electroencephalography 26
Conus medullaris syndrome 87, 91
Echocardiography 66
Coughing, spinal cord injury 92
Embolism
Cranial nerves 5 pulmonary risk factors 46
Crutches 56
Index
Emotional support 52
Cryotherapy Endurance 83
for spasticity management 120 Eye movements 6
Cueing. 81, 82 See optic nerve 5
oculomotor nerve. 6
D
F
Debridement, pressure sores 60
Decubitus ulcers 90 Facial nerve
Deep tendon reflexes 15 see cranial nerve VII 6
Deep vein thrombosis 89 Facial palsy
Deep breathing exercise 96 See for bell's palsy treatment 34
Deltoid muscle innervations 11 Family history 3
Index 139
H Jaw reflex 6
Index
Short term 4 O
Meningeal irritation, test for
ORLAU hip guidance orthosis
kernig's sign 8
(HGO) 125
MCA (Middle cerebral Artery) 42
Orthosis
Medical complications
use, in cerebral palsy 124
see spinal cord injury 89 stroke 40
Medical research scale (MRC) 9 spinal cord injury 86
Milwaukee brace 126 muscular dystrophy 64
Mini- mental examination 3 Occupational therapist, 121
MMT (Manual muscle testing) 9 cerebellar ataxia 116
Mobility transfer 96 Ocular examination 6
Wheel chair mobility 97 Oculomotor nerve III 6
Index 141
heterotopic ossification 89 T
spinal orthosis 97
rehabilitation for Task related training 51
assistive device 98 Tapping technique
Scoliosis 126 see shoulder subluxation
Sensation 19 in hemiplegia 58
TENS (transcutaneous electrical
Skin sensation 19
stimulation) 99
Sensory dermatomes 19
Temperature sensation 19
Sexual dysfunction 95
Treadmill walking with body
Shoulder pain support 54, 112
cerebrovascular accident 57 Trigeminal nerve
Spasticity (hypertonia) 13 see cranial nerve V 6
Speech Trochlear nerve
communication problems 5 see cranial nerve IV 6
Spinal orthosis Trunk instability 81
lumbosacral orthosis 126 Tetraplegia
TLSOs (thoracolumbosacral transfer training in spinal cord
orthoses) 126 injury 95
cervical orthosis 126 in stroke 52
four poster brace 125 Transient ischemic attack (TIA) 40
halo brace 125 Tremor 77
Jewett hyperextension Two point discrimination 20
device 125
Soft collar 126 U
SOMI brace 126 Ulcers
Thoracolumbosacral see pressure sores 59
orthosis 126 Unconscious patient 3
Splint UMN (upper motor neuron) 45
in cerebral palsy 102 Upper limb orthosis 126
in hemiplegia 55 Ultrasonography 60
Index
in muscular dystrophy 70
in talipes equinovarus 104 V
Standing frame 98
Stretching 68 Vagus nerve
Stroke 44 see cranial nerve X 7
Vascular problems 42
Subarachnoid hemorrhage 40
Ventilation assistance support 72
Superficial thrombophlebitis 88
Vertebral artery 42
Swallowing disorder Vertebrobasilar distribution
see dysphagia 79 ischemia 41
Vestibulocochlear nerve VIII cranial
nerve 7
Index 143
Index