3 cases of paraparesis
Hello all, I am a final MBBS part II student, and this is a log of learning points from three cases of paraparesis. This is to complete my log book as a part of under graduate course
Case 1
List of problems
Limb weakness at lower limb, Started 2 years back insidious oncet of gradually progressive and progress to distal region
Possible causes of problems
Limitation of function due to Jointor stiffness
Impaired motor activity because of Severe proproseptive sensory loss
UMN lesion
LMN lesion
Myopathy could
Psychogenic
Clinical signs help in differentiating these causes are
Atrophy
Fasciculations
Tone
Distribution of weakness
Muscle stretch reflexes
Babinski sign
In this particular case there is
no atrophy of muscles and
tone is normal
distribution of weaknesses is proximaland later developing distal weakness
muscle stretch reflexes are absent
Babinski is absent
disease shows no variation in time and it is progressive
so this indicates a myogenic or neurogenic cause
Myopathic causes
Which can be further divided into neuromuscular junction weakness and muscle weakness in this case neuromuscular junction is ruled out because there is no fatigable weakness
Myopathic weakness is produced by a loss of muscle fibres which is caused by
- Muscular dystrophy
- Inflammatory myopathy
- Necrosis of muscle fibres
Considering the distribution of weakness paraparesis the causes for this paraparesis
- trauma to Lower back producing Cauda equina
- Disc herniation
- Intrinsic spinal tumour in this urinary sprinters are affected producing autonomic bladder or neurogenic bladder
- Rarely weakness of bilateral lower limb this is caused by anterior horn cell Disease and peripheral neuropathy
Upon clinical examination persistent weakness presence with one of the seven patterns of these two patterns are particularly important for this case these are
1. proximal weakness more than distal weakness
- Immune mediated necrotising myopathy
- Polymyositis
- Dermatomyositis
- Muscular dystrophy
- mitochondrial myopathy
- Toxic myopathy
- Endocrine myopathy
2. proximal and distal
- Inclusion body myosotis
Specific clinical features for differential diagnosis
- Polymyositis - myalgia + weakness
- Inclusion body myositis - age more than 65 years distal upper excremity is also involved
- Dermatomyositis - Slow onset proximal weakness, dusky patches knuckle and knee also known as gottron sign and Periorbital Lialac colour and dysphagia
- muscular dystrophy - pelvic muscles first involved next shoulder muscle and calf muscle pseudohypertrophy, older individuals have associated cardiomyopathy and cognitive impairment, hyperlordotic gait, Gowers sign: uses arms to get up.
- Endocrine myopathy - observed in hypothyroidism and hyperthyroidism hyperparathyroidism, hyperparathyroidism, Cushing, pituitary disease, diabetes mellitius.
Diagnostic approach
spinal MRI
This is done considering spinal tumours disc herniation
electromyography
- irritability on needle insertion suggest a necrotising myopathy
- No irritability after needle insertion suggest a chronic inflammatory disease such as muscular dystrophy
- Reduction in muscle contraction amplitude on repetitive stimulation suggests neuromuscular junction disorder
- Presence of short duration small amplitude polyphasic motor unit action potential suggests a neurogenic disorder or loss of type too fast twitch fibres, Reduction in small amplitude polyphasic motor unit action potential and suggests myopathic disorder
Nerve conduction velocity
Electro cardiogram, chest x-ray considering muscular dystrophies
We would find features of dilated cardiomyopathy
Creatinine kinase MM levels, AST, ALT, LDH LEVELS
Elevation suggest muscle damage
muscle biopsy
Thyroid profile
Neuropathic cause
Clinical signs help in differentiating different neuropathic causes
- motor of sensory to a gnomic make
- Distribution of weakness
- Type of sensory involvement
- Any upper motor neuron loss
- Acute / chronic / subacute
- Any family history
- Associated chronic diseases
This case there is a symmetric proximal and distal weakness so considering CIDP, spinal muscular atrophy
Diagnostic approach
Electro diagnostic tests
LFT
RFT
fasting blood glucose
HB A1 C
complete urine analysis
thyroid profile
Vitamin B12
Folio acid
antinuclear antibody
Serum protein electrophoresis
Nerve a biopsy
Diagnosis
1)Anatomical location of the root cause
- Peripheral nerves Schwann cells
2) Physiological functional disability
- Demyelination causing nerve conduction abnormality
3) Biochemical abnormalities that could be a root cause at a molecular level
4) Pathology that could reflect the root cause at a cellular level
Solutions to tacle root causes
- Corticosteroids
- Intravenous immunoglobulin
- if both are inefective plasma exchange
- Rituximab, azathioprine
recent advances
Case 2
List of problems
Difficulty in walking, Climbing stairs since 1 month.
Bilateral lower limb weakness since 1 month
Difficulty in holding chappal
Wasting and thinning of lower limb muscles more than the upper limbs.
Examination findings
reduced bulk of all the four limbs.
Hypotonia of lower limbs (LMN lesion)
Absent plantar reflexes (LMN)
Clinical signs help in differentiating different neuropathic causes
- motor or sensory
- Distribution of weakness
- Type of sensory involvement
- Any upper motor neuron loss
- Acute / chronic / subacute
- Any family history
- Associated chronic diseases
LMN paraparesis is suspected because
- Reduced tone bilaterally
- Bilateral wasting and weakness
- Reduced reflexes
- Unable to walk
- No sensory loss
- No cerebellar signs.
There were no fasciculations to suggest motor neuron disease
No limb shortening to suggest Polio
No ptosis or ophthalmoplegia or facial weakness to suggest Gullian barre syndrome or Myasthenia.
No Pes cavus or toe clawing to rule out Charcot Marie Tooth Disease.
Suggest diagnosis of peripheral neuropathy, mononeuropathy multiplex
Multiple mononeuropathies (mononeuropathy multiplex)
suggest a patchy multifocal disease process such as vasculopathy (eg, diabetes, arteritis), an infiltrative process (eg, leprosy, sarcoidosis), radiation damage.
Diagnostic approach
Creatinine kinase was normal (Rule out Myopathy)
Subacute combined degeneration of spinal cord is ruled out by perepheral blood smear.
Infections were excluded.
After Nerve Conduction Studies, Polyneuropathy involving common peroneal and sural nerves was found.
Complete blood cell count
Renal function
Liver function tests
Erythrocyte sedimentation rate (extractable nuclear antigen if dry eyes/mouth and sensory neuropathy are present)
Fasting glucosea (11%) or hemoglobin A1ca (26%)
Thyroid stimulating hormone
Monoclonal proteina (serum protein immunofixation electrophoresis) (10%)
Vitamin B12 (2%) (with methylmalonic acid 9%)a
Infectious (if risk factors or endemic region): Lyme disease, human immunodeficiency virus
Family history of peripheral neuropathy, pes cavus.
Case 3
List of problems
Weakness of both the lower limbs associated with tingling and numbness since 5 days.
Vomiting 3 episodes 5 days back non bilious.
Gluteal abscess
Scrotal abscess which was drained 10 days back
Examination findings
There was bilateral loss of power and hypotonia, Reflexes were present and Ankle clonus was present. Suggests a UMN lesion in cortex as both upper limbs and lower limbs were effected.There were no meningeal signs like neck stiffness or kernigs or brudzinkis sign.
Routine chest X-ray was done and multiple nodules on the apical lung were found suggestive of military TB.
MRI shows ring enhancing lesions in right and left cerebral hemispheres in the parasaggital area, in the ACA territory. Bilateral appearance of this led to the suspicion of vasculitis triggered by TB infection given the history of disseminated TB infection.
Diagnostic approach
Mantoux test: positive in TB
Lymph node biopsy
Lumbar puncture and CSF Analysis (for features of Froin’s loculation syndrome)
Serum vitamin B12 levels
Electromyography (muscles will be affected in motor neuron disease)
Nerve conduction study (to differentiate between motor neuron disease and peripheral neuropathy)
Management
ATT 3 tabs/day fdc
Benadon 40mg/od
pregabalin 75mg/po/h/s
Oint.megaheal for local application
Sitz bath with betadine tid (For the gluteal abscess)
Frequent change
Additional management
In caries spine:
Application of traction in early stage.
“plastic jacket” is applied for immobilization.
Physiotherapy:
Passive movements are carried out in the lower limbs once or twice daily.
Later on, arrangement of wheel chair, walking calipers are done according to the necessity.
Surgery:
Drainage of cold abscess
Laminectomy for caries spine.
References
1. Harrison principles of internal medicine
2. Davidson principles and practice of medicine
3. Current medical diagnosis and treatment
4. Hutchinson clinical methods
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