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A 13 years old girl Tehmina d/o Mehmood, unmarried, resident of Orangi Town, Karachi, with no known co-morbids, presented in ER with the complaints of:
According to the patient, she was alright 1 month back, then she developed high-grade, intermittent fever, with rigors and chills. Fever spike occurred almost daily in the evening. There was no associated cough, urinary problem, shortness of breath, rash, sore-throat, change in bowel habits, severe fatigue, yellowish discoloration of sclera.
She took anti-malarials and anti-pyretics from a doctor, and the fever started to resolve. But she noticed mild to moderate pain in her Left Leg on 1st of September, followed by weakness in her Left Leg, which progressed rapidly to complete loss of power in her Left Leg.
Then she developed mild pain in her Right Leg within 12 hours of Left Leg weakness and had complete weakness in her Right Leg too, followed by urinary retention and constipation
On the day of the weakness, she was taken to a local Doctor, who gave her Inj Mecobalamin, Inj Novidat, and Tab Deltacortil 3 OD And then referred to CHK
No h/o any confusion or altered consciousness, limb weakness or numbness, double vision, pain in eye, headache, trauma to head or back, difficult in swallowing or speaking, dizziness, tinnitus, gait or balance problem, vomiting, drooping of eyelid, improvement in weakness after rest No h/o any rash, mouth ulcers, hair loss, arthralgias
and a local GP advised to transfuse blood. No labs available No h/o jaundice, blood loss, worms infestation, dietary preference or avoidance
No h/o weakness, visual loss, sphincter disturbance, dizziness, gait disturbance in the past
Student of class 7th as well as Madrassa student Sleep disturbed ( no obvious cause) Appetite reduced No diet preferences or avoidance Constipated Foleys catheter passed due to retention
No h/o similar weakness in any family member Father died of heart trouble 5 years back Mother and 3 brothers alive and healthy
Next door neighbour had Pulmonary TB and our patient used to visit her frequently
Lower class
Young adolescent girl of average height and lean built, lying comfortably on the bed, conscious and oriented to time, place, and person. BP = 100 / 60 mmHg Pulse = 100 / min Regular RR = 18 / min T = 98.8 degree F
No evidence of anemia, jaundice, cyanosis, clubbing, dehydration, edema Thyroid not palpable Lymph nodes not enlarged JVP not raised
Bulk Normal Tone Reduced in both lower limbs Power 0/5 in both Lower Limbs ( hips, knees, ankles, and toes) Reflexes 0 /4 ( even after reinforcement) Superficial reflexes Plantars and Abdominal reflexes absent Gait CNBA Coordination CNBA
Intact
Unremarkable
A young girl presented with rapid onset of bilateral complete leg weakness with urinary retention and constipation, preceded by 1 month of febrile illness. On examination, she is alert, vitally stable. She has 0/5 power in both lower limbs, with hypotonia and areflexia on DTRs and abdominal reflexes, mute plantars, but with intact sensations including perineal sensations. Rest of the examination is unremarkable
Neuropathy ( Motor and Autonomic) / GBS Cauda Equina/ Conus Medullaris Syndrome Spinal Cord Anterior Horn Cell Disorder Myelitis Multiple Scrleosis ( 1st episode)
Hb 9.8 gm% MCV 93 fl TLC 8600 / cubic mm Platelets 620,000 / cubic mm UCE, LFTs, INR WNL HBsAg , Anti HCV Ab Non-Reactive ESR 44 mm in 1st hour CXR
Asymmetric Sensorimotor Axonal Polyneuropathy more marked on Lower Limbs Sural Nerves - Unrecordable Advised to repeat NCS after one week
Abnormal signal intensity changes seen in the lower dorsal cord parenchyma, with slight dilatation Axial images reveal hyper-intense signals in the cord, with the possibility of septations Thoracic cord meninges are also hyperintense, suggestive of Arachnoiditis
Tuberculous Myelitis
as Acute Flaccid Paralysis and Sphincter disturbance with Axonal Polyneuropathy
Retrospective Localization of the Lesion D/D of Acute Flaccid Paralysis Why not a Simple Polyneuropathy? Cauda Equina vs Conus Medullaris syndromes Transverse Myelitis Diagnostic Criteria Myelitis with Polyneuropathy Neuropathy with TB
Findings are consistent with LMN lesion in Lower limbs with sparing of the Upper limbs So it can by any LMN disorder localized to Lower limbs i.e.
Anterior Horn Cells of the spinal cord Peripheral Neuropathy NMJ disorder Muscle disorder
Brainstem Stroke , Encephalitis Acute Anterior Poliomyelitis Acute Myelopathy ( Cord SOL / TM) Neuropathy ( GBS, Post-Vaccination, Diphtheria, Heavy Metals, Vasculitis, Critical Illness) NMJ disorders ( MG , LES) Muscle Disorders ( Hypokalemia, Hypophosphatemia, Inflammatory myopathy, Rhabdomyolysis, Periodic Paralyses)
Hughes RAC, Comblath DR. GBS. Lancet. 2005: 366: 1653 - 66
According to the standard teaching practices: Following features are NOT a feature of Polyneuropathy:
UMN signs Unilateral face, arm, leg signs Prominent Bowel or Bladder disturbance Sensory level Hyperventilation
( Harrisons Principles of Internal Medicine 17th ed: pg 2653: t379-2 )
Although 5 10% of GBS cases have bladder involvement , this is an exception, rather than a rule Prominent bladder involvement is feature of:
Spinal cord problem ( with LMN at the level of
lesion and UMN below the level) Frontal lobe disorder ( with UMN signs in LL and behavioral, speech, gait disturbances)
Sensory Level
Radicular pain
Low back pain
Less severe
More
More severe
Less
Numbness tends to be more localized to perianal area; symmetrical and bilateral; sensory dissociation occurs
Numbness tends to be more localized to saddle area; asymmetrical, may be unilateral; no sensory dissociation; loss of sensation in specific dermatomes in lower extremities with numbness and paresthesia; possible numbness in pubic area, including glans penis or clitoris Asymmetric areflexic paraplegia that is more marked; fasciculations rare; atrophy more common
Motor strength
Typically symmetric, hyperreflexic distal paresis of lower limbs that is less marked; fasciculations may be present
Impotence
Frequent
Less frequent; erectile dysfunction that includes inability to have erection, inability to maintain erection, lack of sensation in pubic area (including glans penis or clitoris), and inability to ejaculate
Sphincter dysfunction
Urinary retention and Urinary retention; tends atonic anal sphincter to present late in course cause overflow urinary of disease incontinence and fecal incontinence; tend to present early in course of disease
1. Acute transverse myelitis and acute motor axonal neuropathy developed after vaccinations against seasonal and 2009 A/H1N1 influenza.
Sato N, Watanabe K, Ohta K, Tanaka H.
3. Simultaneous central and peripheral nervous system involvement in systemic lupus erythematosus.
Ilniczky S, Kamondi A, Arnyi Z, Vrallyay G, Gaal B, Szirmai I, Nagy G.
Such dual lower motor neuron pathology may be associated with a poorer outcome, and indicates simultaneous central and peripheral immune-mediated injury. There may be a place for combined therapy with immunoglobulin and corticosteroids in patients with transverse myelitis and inflammatory neuropathy.
The causes of peripheral neuropathy associated with tuberculosis may be: 1. Immune-mediated neuropathy 2. Direct invasion of nerves 3. Granulomas in the peripheral nerve 4. Vasculitic neuropathy 5. Compressive neuropathy 6. Meningitic reaction 7. Toxic effects of antituberculous chemotherapy.
Neuropathy occurs as a complication of meningitis, causing spinal nerve root and cranial neuropathies (especially cranial nerves II, III, VI, VII, and VIII).
Cranial nerve involvement may result from longstanding increased intracranial pressure, direct effects of the tuberculous exudates on the nerve, and arteritis of the nerve root, within exudates, has been described.
Isolated tuberculomas in the optic nerve have been reported.
Local pressure in the nasopharynx (cranial nerves IX, X, and XI palsies), in the middle ear and mastoid (cranial nerve VII palsy and hemifacial spasm), and chest (recurrent laryngeal nerve palsy), have all been observed. Carpal tunnel syndrome may result from tuberculous tenosynovitis in the hand. The association of tuberculosis with Guillain-Barre syndrome is uncertain, although patients have been reported with both conditions coexisting. This may be a chance association.
INH induced Polyneuropathy: initially sensory, later motor with features of axonal degeneration.
This should be prevented by coadministration of pyridoxine.
Repeat CSF after 10 days ( as advised by Prof Dr Yasmeen) Repeat NCS after 1 week (as advised by NCS department)
Thank You