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paraparesis case- 1

Hello everyone,I am a fourth year MBBS student.I have been given this case to share my views regarding pathophysiology,diagnosis and treatment options in cases of paraparesis.

Detailed clinical history and investigations of the patient are in the following links :

UNDERSTANDING THE CASE

This a case of bilateral symmetrical lower limb weakness.
  • Weakness started in proximal region and then gradually progressed to distal region.
  • Proximal muscle weakness since difficulty in squatting and getting up from that position. Distal muscle weakness suggested by difficulty in wearing and holding chappals.
There is no weakness in the upper limbs and there is no cranial nerve involvement.

Distribution of weakness:Both lower limbs:PARAPARESIS.

No history of sensory loss.

Areflexia in both lower limbs.

ANATOMICAL LOCALIZATION OF SITE OF LESION:

Weakness can be due to both upper and lower motor neuron lesions.
Features of upper motor neuron lesion are:
  • SPASTICITY
  • Hypertonicity
  • Hperreflexia
  • Disuse atrophy (minimal)
  • Positive babinski's sign
Features of lower motor neuron lesion are:
  • FLACCIDITY
  • Hypotonicity
  • Hyporeflexia
  • Denervation atrophy(profound)
  • Negative babinski's sign
  • Fasciculations are present
In this patient there are no features suggestive of upper motor neuron lesion.

LOWER MOTOR NEURON: These are the alpha and gamma motor neurons in the anterior horn of spinal cord.
Axons of lower motor neurons travel peripherally to innervate muscles.Sites of lower motor neuron include:
  1. ANTERIOR HORN CELL 
  2. SPINAL NERVE ROOT(radical) AND PLEXUS
  3. PERIPHERAL NERVE
  4. NEUROMUSCULAR JUNCTION
  5. MUSCLE
AHC LESION
  • No sensory/autonomic/cerebellar invovement.
  • Different patterns of weakness.
Asymmetric distal weakness without sensory loss:ALS(amyotrophic lateral sclerosis),PLS(primary lateral sclerosis),MMA(monomelic amyotrophy).
Symmetric weakness without sensory loss:PLS,PMA.
  • Lower motor neuron signs like weakness,wasting and fasciculations with/without UMN findings.
RADICULOPATHY AND PLEXOPATHY
  • Usually ASYMMETRICAL
  • Root pain is present along the distribution of nerve.
  • Sensory,motor systems involved and areflexia seen.
  • Muscles supplied by that particular nerve root are involved.
PERIPHERAL NEUROPATHY
  • Sensory and motor invovement seen.
  • Ususally distal to proximal evolution of the disease.
They can be AXONAL or DEMYELINATING neuropathies.
 
AXONAL NEUROPATHY
It is a chronic polyneuropathy with distal to proximal evolution.Reflexes are usually spared unless it is a large fibre neuropathy.
There is predominant sensory involvement.
DEMYELINATING NEUROPATHY
It has a acute to subacute presentation and is a polyradiculoneuropathy.
There is diffuse proximal and distal muscle involvement.
Reflexes are lost.
There is predominant motor involvement.Sensory system if involved is mainly dorsal column involvement.

NEUROMUSCULAR JUNCTION LESION
  • Fatiguability.
  • Fluctuating weakness.
  • Ocular/pharyngeal muscle involvement.
MYOPATHY
  • Pure motor weakness.
  • Predominant proximal muscle involvement.
  • No fasciculations.
  • Reflexes are preserved.
With the above references I would like to mention the following differentials:
  1. MYOPATHY
  2. DEMYELINATING POLYNEUROPATHY
PATHOLOGY AND ETIOLOGY OF MYOPATHY:
Myopathy refers to muscle disease resulting in muscle weakness.
Weakness can be episodic or constant.In this case it is a constant weakness.
CONSTANT WEAKNESS:
  • INHERITED OR ACQUIRED MYOPATHIES.
Inherited muscle disorders are called muscular dystrophies:
  1. Duchenne's muscular dystrophy
  2. Becker's muscular dystrophy
  3. Limb girdle muscle dystrophy
  4. Emery Dreifuss muscle dystrophy
  5. Fascioscapulohumeral muscle dystrophy
  6. Myotonic dystrophy
  7. Mitochondrial myopathies
Dystrophinopathies(Duchenne and Becker's) are likely in this case.
  • Both have X-linked recessive inheritance due to a mutation in dystrophin gene.
  • Duchenne muscular dystrophy is a more severe form usually presenting before the age of 5. Proximal muscles of lower limbs are predominantly involved with positive gower's signThere is pseudohyperthrophy of calf muscles.They do not live longer because of serious cardiac conduction abnormalities and dilated cardiomyopathy.Therefore,Duchenne is unlikely in this patient.
  • Becker's usually survive into their 40's and have highly variable disease onset.
Acquired myopathies are due to the following causes:
  1. Inflammatory (Polymyositis/Dermatomyositis)
  2. Drug induced
  3. Endocrine
ADDITIONAL INVESTIGATIONS:
  1. Creatinine phosphokinase levels;Increased in dystrophies.
  2. Electromyography
  3. Genetic testing
  4. Nerve conduction study:Demyelinating neuropathies show slowing of conduction velocities, prolongation of distal latency.
  5. Muscle biopsy 
THERAPEUTIC OPTIONS:

  1. Steroids may help in slowing the muscle degenerative process.
  2. Physiotherapy.
  3. ACE inhibitors/ARB's /Beta blockers to manage his cardiomyopathy.



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