PARAPARESIS 3

I've been given this case
https://vaish7.blogspot.com/2020/05/medicine.html
 to solve in an attempt to understand the topic of "paraparesis."

This may develop my competency in

a) reading and comprehending clinical data related to "paraparesis" including history, clinical findings, investigations

b) come up with a diagnosis such as:
1) Anatomical location of the root cause
2) Physiological functional disability
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

c) a treatment plan for each of these patients of paraparesis that can have a pharmacological and non pharmacological component.

d) learning the scientific basis of diagnostic and therapeutic approach in terms of past collective experiences and experiments (aka evidence based medicine).

Following is my analysis of patient's problem.

A 23 yr old male patient presented with complaints of  bilateral weakness of lower limb since 5 days and gluteal abscess since 5 months.


Based on history

There are no involuntary movements and cerebellar involvement.He has a history of tingling and numbness.So there maybe sensory,LMN OR UMN involvement.

Based on examination


  • Findings suggestive of  UMN lesion in this case are exaggerated deep tendon reflexes , ankle clonus is present and babinski is up going(positive).
  • Finding that are suggestive of LMN lesion in this case are hypotonia.
  • There is no sensory involvement.
Most of the features are suggestive of UMN lesion .But then what about  hypotonia??As the pathology is still in initial stages there may be hypotonia in some cases of UMN lesion. So I think pathology of this case is related to UMN LESION.

As UMN consists of mainly corticospinal tract which extends from cerebral cortex( primary motor cortex, premotor cortex,post central gurus),internal capsule, pons, mid brain, medulla to spinal cord (anterior gray matter).Now where exactly is site of lesion.??

On further examination all the cranial nerves are intact this excludes brainstem involvement. I exclude internal capsule lesion because if it is involved then most of the body should be affected (hemiparasis) but in this case it is Paraparesis.Now we are left with cortical and spinal cord involvement.

One of the possibility of CORTICAL involvement:

As there is weakness of lower limbs there may be related to vasculitis of anterior cerebral artery.But this case can be ruled out as MRI brain did not show any of the features.

One of the possible explanation for Spinal cord invovement:

In this case patient has a history of gluteal abscess.According to this my analysis, there must be underlying tubercular infection that lead to Pott spine.Spread of infection in this case could be to lumbar vertebra which caused causing damage to vertebra and disc leads to spinal cord damage mostly at L3-L4 spinal segments which lead to paraplegia of lower limbs.This could also be the reason behind gluteal abscess.
https://en.wikipedia.org/wiki/Pott_disease
Investigation that can be done are:

  • Sputum microscopy
  • MRI of spine
  • Lumbar puncture
  • Culture can done from abscess to check for tubercular bacilli
Investigation performed are:
  • MRI brain which showed ring enhancement lesion.
Treatment 
  • Antitubercular drugs 
  • Abscess drainage








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