PARAPARESIS

I've been given these three cases data here (https://medicinedepartment.blogspot.com/2020/05/case-based-online-learning-assignment.html?m=1) to solve in an attempt to understand the topic of “paraparesis”

Hereafter,

https://vaish7.blogspot.com/2020/05/medicine.html?m=1 

This case will be referred to as Case 1

https://hitesh116.blogspot.com/2020/05/elog-13th-may-2020.html?m=1 -

Case2

https://hitesh116.blogspot.com/2020/05/12may-2020-elog-medicine-intern.html?m=1 

Case 3

Paraparesis is defined as partial paralysis of lower limbs.

In case 1, 

The complaints of the patient were :

• Weakness of both the lower limbs associated with tingling and numbness since 5 days.
• Vomiting 3 episodes 5 days back non bilious.

When a patient presents with complaints of lower limb weakness,

We first try to distinguish true muscle weakness from lassitute or motor impairment not due to loss of muscle power.

Lassitude describes the inability to continue performing a task after multiple repetitions but a patient with primary weakness is unable to perform at the first repetition of the task.

We can attribute to Primary weakness in our patient.

 The primary muscle weakness can be divided into many categories

1. Infectious
2. Neurological
3. Endocrinal
4. Inflammatory
5. Rheumatological
6. Genetic
7. Metabolic
8. Electrolyte Induced
9. Drug induced

• Detailed history of the patient included onset and progression of the weakness, if it is global or focal, proximal or distal can differentiate between various causes of lower limb weakness.

          Acute - Infection or Stroke

          Subacute - Drugs, Electrolyte imbalance, Inflammatory, Rheumatologic disease.

          Chronic - Genetic and Metabolic Myopathies

• Physical examination of the patient for associated symptoms gives an account of the cause.

We can tell that it is neuroplegia which is acute, bilateral,  associated with distal muscle weakness.

The associated history of

Gluteal abscess for which he was operated 5 months back

Scrotal abscess which was drained 10 days back

Gives us the idea of infectious etiology.

On examination,

There was bilateral loss of power and hypotonia, Reflexes were present and Ankle clonus was absent.

Routine chest X-ray was done and multiple nodules on the apical lung were found suggestive of military TB.
There were no meningeal signs like neck stiffness or kernigs or brudzinkis sign. With this we can rule out infectious meningitis. (TB Meningitis)

To find out if the neuropathy is Central or Peripheral an Xray abdomen was done and it showed a psoas abscess on the left L5 and L4 which we can attribute to paraparesis. But there was no loss of reflexes. So a LMN lesion is ruled out. The peso as abscess wasn’t the cause of paraparesis.

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.
*Differential diagnosis of flax cerebral tuberculoma was also made. But the MRI appearance wasn’t suggestive of a tumour. It was diffuse and bilaterality of the cortical lesion arises the suspicion of a vascular cause.
According to homunculus, the medial surface area supplied by ACA controls the lower limb and hence the paraparesis of the lower limb.

A very few cases were reported with such complications one of them is https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4606267/
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In Case 2,

The patient presented with the following main complaints-

• 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.

On examination,

The patient had reduced bulk of all the four limbs.

Hypotonia of lower limbs (LMN lesion)

Absent plantar reflexes (LMN)

Creatinine kinase was normal (Rule out Myopathy)

Subacute combined degeneration of spinal cord is ruled out by perepheral blood smear.

Infections were excluded.

• Flaccid paraparesis is suspected. (LMN)

- 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 sensory level to suggest Cauda Equina

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.

• DD of peripheral neuropathy was made.

After Nerve Conduction Studies, Polyneuropathy involving common peroneal  and sural nerves was found.

Peripheral neuropathy 

Peripheral neuropathy refers to disorders of the peripheral nervous system.
The initial step is to confirm whether the signs and symptoms are related to peripheral nerve dysfunction.
Spinal cord disease is the most common differential diagnosis in patients with neuropathic symptoms. In patients with myelopathy, the sensory symptoms are present with few clinical signs; the classic signs of lower motor neuron involvement may be absent, simulating peripheral neuropathy.
Patients with lacunar stroke may rarely present with sensory loss in median or ulnar nerve distribution. 
Although patients with spinal canal stenosis present classically with neurogenic claudication, in advanced stage, they may be associated with persistent symptoms and the condition may be confused with peripheral neuropathy.
In elderly patients, often there is a coexistence of cervical spondylotic myelopathy with late onset predominantly sensory axonal neuropathy. Similarly, spondylotic radiculopathy may occur with upper limb entrapment neuropathies, and the coexisting pathologies should be carefully diagnosed. Neuropathy may also occur with CNS involvement in vitamin B12 deficiency, adrenomyeloneuropathy and acanthocytosis.
The peripheral nerves comprise sensory, motor and autonomic fibers, which have different lengths, diameters, conduction characteristics and specialized functions. Their involvement therefore results in diverse symptoms, signs and EDx features.(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771953/)

Since sural and peroneal nerves are involved it’s a mononeuritis multiplex which might have occured because of Leprosy, Systemic vasculitis.
To identify the cause of this condition, a sural nerve biopsy was ordered.
Biopsy can detect a vasculitic pathology or Chronic Inflammatory Demyelinating Polyneuropathy.
Biopsy results awaited.
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In Case 3,
The chief complaints were -

• Weakness of lower limb since 20 days. Which started proximally 2 years back later spread distally.
• Difficulty in getting up from squatting position (Proximal muscle weakness)
• Bilateral edema of lower limb - non pitting type
• Difficulty in wearing and holding chappal

On examination, the Cranial nerves are intact and Motor system has a Normal tone, Reflexes are absent.
No Meninges and Cerebral signs.
We attribute the above features to Myopathy rather than Neuropathy.
Myopathies are disorders affecting either the channel, structure or metabolism of skeletal muscle. 

The differences between neuropathy and myopathy are as follows :

	Neuropathy	Myopathy
Site of weakness	Distal weakness	Usually proximal
Sensory	May have concomitant sensory symptoms and signs	Usually pure motor
Reflexes	Reflexes lost early	Reflexes preserved till late
Fasciculations	Fasciculations may be present	Not typical
Contractures	Contractures not a feature	Contractures present
Myocardial dysfunction	Not a typical feature	May have accompanying cardiac dysfunction with the dystrophy

After localising the lesion to the muscle, we need to know if it is 
1. The pathology of muscle channel, muscle structure, or a dysfunction in muscle metabolism.

2. Cause of Myopathy.

A pattern recognition approach for Myopathy is given In this link (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4233647/)

A muscle biopsy should be done to know the pathology.
After the biopsy, a DD of Polymyositis or Muscle dystrophy was made.

Polymyositis :
It is a chronic muscle weakness and Inflammation involving the skeletal muscle.
There might be an autoimmune or a Viral cause to it.

Muscular dystrophy :

Muscular dystrophy is a group of diseases that cause progressive weakness and loss of muscle mass. Abnormal genes (mutations) interfere with the production of proteins needed to form healthy muscle.

Duchenne type muscular dystrophy, Beckers Muscular dystrophy which is a milder form of DMD, are the most common types of muscular dystrophy.

Beckers Muscular Dystrophy :

It is an inherited condition that involves progressive weakness and wasting of skeletal and cardiac muscles. It is caused by mutation in DMD gene, inherited in an X recessive manner. It is just a milder form of Duchenne muscular dystrophy.

Treatment is corticosteroids such as prednisone can slow the decline of muscle strength.

Trial for deoxyribose can be done. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5909143/)