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CARPAL TUNNEL SYNDROME (CTS)
A. Characterized by : fluctuating numbness, paresthesia &
pain in the hand due to compression of the median nerve at the
wrist. - 80 % occurs in women.
B. Etiology & Pathology :- Many causes of compression : 1.
Hereditary2. Traumatic3. Infectious.4. Metabolic5. Endocrine6.
Neoplastic7. Vascular8. Degenerative9. Iatrogenic.
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C. Clinical features:- Earliest symptoms: numbness +
paresthesias in the sensory distribution of median nerve in the
hand (thumb, index, middle, and lateral half of the ring fingers).-
Later: pain develops extending up into the forearm & often the
shoulder.- The pain is worse at night. - Late event: weakness
inability to unscrew bottle cap or grip properly.
D. Diagnostic Procedures:1. EMG : reveal fibrillations in the
muscles of the thenar eminence.2. Distal latency of median nerve is
prolonged.3. Sensory nerve conduction velocities & sensory
distal latency are prolonged on stimulating the digital nerves of
the index finger.
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E. Tx: - The area around the nerve is infiltrated with 2- 3 ml
of 1% Lidocaine; followed by an inj of 40 mg Methylprednisolone.-
Fail to respond to inj surgical division of the transverse carpal
ligament.
F. Prognosis:- Excellent if the cause is removed / treated.
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TARSAL TUNNEL SYNDROME(POSTERIOR TIBIAL NERVE)A.
Pathophysiology: - Just below the medial malleolus lies a passage
through pass the medial & the lateral plantar nerves.- In cases
of excessive pronation of the foot, the load increases in the
tissues that surround the flexor tendons inflammation swelling
trapping of these nerves.B. Diagnosis :The pain may be aggravated
by pressure over the posterior tibial nerve just below & behind
the medial malleolus.C. Tx:- Infiltration of the tarsal tunnel with
1 % Xylocaine, followed by 40 mg of Methylprednisolone (Medrol).-
In intractable cases Surgical.
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References:
1. Peterson, L; Renstrom, P. Sport Injuries : Their prevention
and treatment: 1988; p.363 .2. Gilroy, J. Basic Neurology.
International Edition:1992; p. 371
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MYASTHENIA GRAVIS (MG)
A. Background:- Myasthenia gravis is an autoimmune disease
caused by an immunologic attack directed against the postsynaptic
neuromuscular junction (NMJ).- can occur at any age.- sometimes
associated with rheumatoid arthritis, disseminated lupus
erythematosus.- 70 % have thymic hyperplasia.- 10 % have
thymoma.
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B. Pathophysiology:MG is an acquired autoimmune disorder of
neuromuscular transmission resulting from antibodies directed
against the acetylcholine receptor (AChR) or against the
muscle-specific receptor tyrosine kinase (MuSK).
C. Dx :- Clinical feature: Fluctuating weakness characterized by
abnormal fatigability that improves with rest.
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D. Testing: - Tensilon (Edrophonium) test can be helpful in
diagnosing MG.Edrophonium is an anticholinesterase and will result
in transient increase in AChR in NMJ. Edrophonium is given I.V.
Dose is 10 mg(1 ml) : * 2 mg is given initially. * The remaining 8
mg: approximately 30 seconds later if the test dose is well
tolerated. There is an obvious improvement in the strength of weak
muscles that lasts for about 5 minutes.
E. Clinical features:- Fluctuating weakness. - Tends to involve:
* the eyes in 90% of Pts.(diplopia, ptosis). * face, neck &
oropharynx: 80 % * limbs: 60 %.
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F. Tx :- Acetylcholinesterase inhibitors: #
Pyridostigmine(Mestinon): start with 4x 30 -60 mg (the dosage is
gradually titrated). Most adults require 4-6x 60-120 mg.# Mestinon
Timespan (is a timed-released): 180 mg can be given at night for
Pts who have generalized weakness upon awakening.-
Immunosuppressive- Plasma Exchange (PE).- Thymectomy.
#. Ref.:1. On Call Neurology, 1997, pp.198 201.2. Gilroy, J.
Basic Neurology. International Edition, 1992.3. Greenberg, DA et
al. Clinical Neurology 7th. Ed. The McGraw-Hill Companies, Inc.
2009, pp. 185 188.
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HYPOKALEMIA
A. Background:- is defined as a serum potassium (K) level below
3.5 meQ/L.B. Pathophysiology :1. Because of abdominal intracellular
or extracellular potassium balance or excessive potassium losses
(renal or extra renal). 2. Due to excessive cellular potassium
uptake.3.Extrarenal potassium loss (urine K < 20 mEq/d) may be
caused by: - Diarrhea - Cathartics; sweating. - Vomiting4. Renal
potassium loss (urine K > 20 mEq/d) may be due to: -
Hyperreninemia - Diuretic use.- Hyperaldosteronism. -
Hypomagnesemia- Renal tubular acidosis.
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C. Prognosis:- Severe hypokalemia (serum Potassium < 1.5 mEq)
may be life threathening due to cardiac arrhythmia and severe
muscle weakness.D. Dx:- The Dx is made with a serum potassium
measurement. E. Tx: 1. Correct Potassium balance problems.2.
Dietary sodium restriction (< 80 mEq/d) will reduce renal
potassium losses.3. Oral KCl for mild hypokalemia (30-35 mEq/d).4.
For moderate (1.5-3.0 mEq/L) or severe (< 1.5 mEq/L)
hypokalemia, especially with cardiac arrhythmias and/or severe
muscle weakness, IV KCl at the rate of 15 mEq over 15 minutes with
continuous cardiac monitoring, aiming for a 1 mEq/L increase in the
serum potassium.
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PERONEAL PALSYA. LESION OF THE COMMON PERONEAL NERVE:- Common
peroneal nerve arise in the posterior aspect of the thigh as one of
the two terminal branches of the sciatic nerve.- Injured by: #
penetrating wounds of the lower portion of the posterior aspect of
thigh / popliteal fossa.# involved in fractures of the lower
portion of the femur / head of the fibula.- Symptoms:# Foot drop#
High steppage-gait# Wasting of the muscles of the anterior
compartment of the leg# Sensory loss extending over the lateral
aspect of the leg + dorsum of the foot.
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B. LESION OF THE SUPERFICIAL PERONEAL NERVE:# This nerve arises
at the level of bifurcation of the common peroneal nerve just below
the neck of the fibula.# The nerve down anterior to the fibula
between peroneal & extensor digitorum longus muscles. # Lesions
produce paralysis of peroneal muscles + loss of eversion of the
foot and a tendency to invert the foot on dorsiflexion.# There is
variable sensory loss over the lower lateral aspect of the leg
& dorsum of the foot.
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C. LESION OF THE DEEP PERONEAL NERVE:#. Arises just below the
head of the fibula as one of the two terminal branches of common
peroneal nerve.#. Lesion commonly affected by pressure over the
head of the fibula, often by sitting with legs crossed for a
prolonged period of time. produces weakness of the dorsiflexors of
the foot & extensors of the toes resulting in := foot drop=
steppage gait= weakness of the muscles of the anterior compartment
of the leg= sensory deficit of the 1st & 2nd toes.
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POLYMYOSITISA. DEFINITION :- is an inflammatory disease of
skeletal muscle.- skin involvement dermatomyositis.B. Etiology :
unknown, but is believed by autoimmune reaction initiated by virus
infection, including the AIDS virus.- the condition may be
associated with :* malignancy* rheumatoid arthritis* Sjogrens
syndrome* SLEC. Pathology:- inflammatory infiltration of sceletal
muscle with necrosis of fibers and active phagocytosis.
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D. DIAGNOSTIC PROCEDURES1. May be presents:-
polymorphonucleocytosis.- ESR - lymphocytosis.- Rh. Factor +-
hypoalbuminaemia. - serum muscle enzymes +- anemia.2. EMG myopathic
process, but often present :- fibrillations- positive sharp waves-
bizarre high frequency discharges.3. ECG:- often abnormal.
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E. Tx: (Bradley, 2000; p. 692)1. Corticosteroids:- Prednisone:
initial dose 2 mg/kg, not ecxeed 100 mg.- Significant improvement
the dose is reduced to 60 mg daily or converted to alternate-day
dose.2. An alternative to corticosteroids is Azathioprine (Imuran)
1.5-2 mg/kg,-Cyclophosphamide & Methotrexate maybe effective in
some patients.
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PNP (POLINEUROPATHY)A. ANATOMY OF THE PERIPHERAL NERVES:# MOTOR
NERVE FIBERS originate from the anterior horn cells of the spinal
cord and leave the cord through the anterior nerve root.# SENSORY
FIBERS originate from neurons in the posterior root ganglia and
enter the spinal cord through the posterior nerve root.- The
anterior & posterior nerve roots unite distal to the cord to
form a mixed spinal nerve.- The mixed spinal nerves unite in the
cervical & lumbar areas to form the cervical, brachial &
lumbosacral plexus. Each plexus gives rise to a number of
individual mixed nerves distributed to the periphery to supply: *
Muscle* Skin* Blood vessel
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B. CLINICAL PATTERNS:These include:1. Mononeuropathy:- implies
involvement of 1peripheral nerve.- commonly the result of trauma,
also occurs in:* DM* Infarction of peripheral nerves (e.g., in
polyarteritis nodosa).2. Mononeuritis multiplex:- involvement of
several nerves in a haphazard fashion.- etiology =
mononeuropathy.3. Radiculoneuropathy:- involvement of the nerve
root as it emerges from the spinal cord.- commonly seen with
herniated disks or with epidural masses (e.g.tumor).
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4. Polyradiculitis = Radiculopathy:- Characterized by
involvement of several nerve roots.- Commonly seen in
postinfectious polyneuritis or post-vaccinal polyneuritis.5.
Plexitis:- inflammation of a plexus such as the brachial plexus
brachial plexitis.6. Polyneuritis:- in polyneuritis /
polyneuropathy there is a symmetric involvement of peripheral
nerves.- the commonest causes:* DM* Alcoholism.
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# Neuropathies no matter what their cause & type present
with specific signs & symptoms.- Involvement of motor axons
muscle wasting & weakness atrophy + fasciculations.- Tendon
reflexes depressed / absent.- Involvement of sensory axons
paresthesia / dysesthesia.- Involvement of axons supplying
autonomic function produces: * loss of sweating* alteration in
bladder function* constipation* impotence (in male).
# Causalgia (a very painful peripheral dysesthesia) probably
related to disturbance of autonomic axons in peripheral nerves.
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DMP (Dystrophia Musculorum Progressiva)# Ref.:1. Gilroy J: Basic
Neurology 2nd ed., McGraw-Hill Inc., 1992, pp.383-386.
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DUCHENNE MUSCULAR DYSTROPHY
A. DEFINITION:- is the most common form of progressive muscular
dystrophy.- almost exclusively in young males.
B. ETIOLOGY & PATHOLOGY:- due to an inborn error of
metabolism that produces abnormal cell membranes.- also excessive
collagen formation.
C. CLINICAL FEATURES:- inherited as a sex-linked recessive
trait.- of cases due to spontaneous gene mutation.- Affected
children normal at birth delay in standing & walking GOWERs
SIGN (walk up his lower extremities).
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- Then develops a clumpsy, waddling gait & pseudohypertrophy
of the calf muscles- Has difficulty climbing stairs & rising
from a chair.- Progressive involvement of heart muscle.-
Progressive loss of respiratory reserve- Many Pts die from the
effect of a relatively minor resp.infection.
D. DIAGNOSTIC PROCEDURES:1. Muscle enzymes:- Serum creatine
phosphatase - Serum levels of other muscle enzymes GOT & GPT.2.
ECG: abnormal at early stage initial tachycardia R-wave voltage
+RBBB + deep Q-waves.3. EMG myopathic.4. Muscle biopsy the
establishment of the Dx.
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E. DD:1. Other form of dystrophy.2. Neurogenic muscular
atrophy.3. Polymyositis & dermatomyositis.4. Polyneuritis.5.
Benign congenital myopathies.
F. Tx:1. No specific Tx.2. Physical Tx; obesity should be
avoided.3. Upper resp. tr. infection should be treated.4. Genetic
counseling.
G. PROGNOSIS:- Duchenne muscular dystrophy progressive.- Death
in late teens or early 20s.