Neuromuscular

Disorders
Neurosurgical Operation – Selective
Posterior (Dorsal) Rhizotomy
 To decrease the stimulating inputs from the muscle spindles in the
lower limbs that arrive in the spinal cord via afferent fibers in the
posterior (dorsal) nerve roots.
Cutting 25-50% of fascicles of each posterior nerve roots from the
level of the second lumbar vertebra to the sacrum.
Indicated for children 3-8 years old with mild spastic diplegia and
are ambulatory.
Very few patients with the athetoid type of CP can be helped by
orthopaedic surgery or selective neurectomy.
Rehabilitation
 For CP children who have never been normal.
Have to be done with compassionate, considerate, and
realistic.
CEREBRAL PALSY IN THE ADULT
 Must be carried through to meet the continuing needs of adolescents and adults
whose cerebral palsy will be continued exist with them.
 The hope is these adult have at least reached their potential (with inevitable
limitation).
CEREBROVASCULAR DISEASE AND
HEMIPLEGIA
 Includes all vascular disorders of the brain.
 The most catastrophic complication is sudden and irreversible ischemia of the brain,
producing stroke syndrome.
 Caused by:
 Hemorrhage
 Thrombosis
 Embolism
 Variable residual effects, depending of:
 Site
 Extent of cerebral ischemic area
CEREBROVASCULAR DISEASE AND
HEMIPLEGIA
 The paralysis is flaccid initially, then followed by spasticity, hypertonicity, increased
deep tendon reflexes, and clonus after few weeks.
 The treatment is mainly to improve musculoskeletal function by means of
physiotherapy.
 Musculoskeletal treatment for stroke victims with residual hemiplegia:
 Psychotherapy
 Physical and Occupational Therapy
 Light Braces
 Selective nerve blocks to relieve spasticity
 Tendon transfers to restore muscle balance and improve function.
 Another problem: fall at home  fracture and joint injuries.
CEREBROVASCULAR
DISEASE AND
HEMIPLEGIA
CEREBRO-
VASCULAR
DISEASE AND
HEMIPLEGIA
DISORDERS AND INJURY
OF THE SPINAL CORD
Disorders and Injuries of the Spinal Cord
 Congenital Myelodysplasia
 Associated with spina bifida, had been discussed in Chapter 8.
 Diastematomyelia
 The lower part of the spinal cord and the upper part of cauda equina is
split into two vertical components by a spur that passes backward from
the posterior surface of a vertebral body and transverse the spinal canal.
 Produces a progressive - lower motor neuron type neurological deficit,
involving the lower limbs, bladder, and bowel dysfunction.
 Another associated congenital abnormality: hairy patch, hemangioma,
dermal sinus.
 Confirmation: CT Scan or MRI
 Treatment: laminectomy and congenital spur excision to prevent
progression.
Disorders and Injuries of the Spinal Cord
 Syringomyelia
 Progressive enlargement of an abnormal cavity (syrinx) within the spinal
cord, filled by cerebrospinal fluid under pressure, most commonly in
cervical region.
 Associated with prolapse of cerebellar tonsils through the foramen
magnum of the skull (Arnold-Chiari Malformation).
 Clinical Manifestation:
o Dissociated sensory loss (pain and temperature sensation loss but light
touch, vibration and position sense are preserved),
o Lower motor neuron lesion on upper extremity
o Atypical scoliosis.
 Confirmation: lateral projection of MRI
 Treatment: neurosurgical drainage of the syrinx, neurosurgical decompression
of foramen magnum, correction and stabilization (fusion).
Poliomyelitis
DEFINITION:
Origin: “Polio”, means “infantile paralysis”.

Viral infection that affects the motor cell in the anterion horn cells of the spinal cord
and is capable of producing permanent paralysis.

Preventable by vaccines (Salk and Sabin)

Poliomyelitis
INCIDENCE AND ETIOLOGY:
 Caused by Poliomyelitis Virus (Enterovirus Group).
 The disease was the most frequent cause of crippling in children and adult (in
lesser extent).
 Affects boys more often than girls.
 Affects lower limbs more often than upper limbs.
 Has been rare because of the vaccination programs.
Poliomyelitis
PATHOPHYSIOLOGY:
 The virus enters the body via the gastrointestinal tract and spreads through the
bloodstream to it’s target (anterior horn cell of the spinal cord and brainstem).
 After an incubation period of 2 weeks, the virus attacks the anterior horn cell and
destroys them.
 Can be:
 Abortive / No Symtomps
 Non-paralytic with systemic symtomps
 Paralytic
 The destruction of anterior horn cell produces lower motor neuron type paralysis.
Poliomyelitis
CLINICAL FEATURES AND DIAGNOSIS:
 Prodromal Phase (2 Days).
 Non specific systemic symptomps common to many viral infection (headache, malaise,
generalized muscular aches).
 Acute Phase (2 months)
 Fever, severe headache, reck rigidity / meningeal irritation, painfull spasm, and tenderness at
involved muscles.
 The CSF contains many lymphocytes.
 Followed by flaccid paralysis of muscles innvervated by damaged anterior horn cell with many
extent.
 Recovery Phase (2 years)
 Gradual recovery of any transient paralysis, most occurs in first 6 months.
 Phase of Residual Paralysis
 Persists of the rest of patient’s life and no further recovery can be expected.
 Deformity because of muscle imbalance, muscle contracture, muscle atrophy and retarded
bone growth
Poliomyelitis
TREATMENT:
 No treatment affects the extent of the paralysis or degree of it’s recovery.
 Symtomatic treatment
 Removable splint to prevent contracture
 Recovery phase: active exercise and suitable braces.
 Operative treatment:
o Tendon Lengthening
o Tendon Transfer
o Tenodesis
o Osteotomy near the joint
o Arthrodesis
o Leg length equalization
Poliomyelitis
Poliomyelitis
Poliomyelitis
POST POLIO SYNDROME:
 Occurs at approximately 50% of Polio patients in 1940-1950 who had long-stable
paralysis.
 Increasing muscle weakness, fatigue, and discomfort in the involved extremities
after 20-40 years.
 Theory: gradual degeneration of involved terminal axon.
 Treatment:
 Education
 Exercise
 Braces
 Lifestyle modification