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PARAPARESIS CASE 2

18 YEAR OLD PARAPARESIS CASE-2

Hello everyone.....I am a 4th year MBBS student.I have been given this case to solve in an attempt to understand the topic of paraparesis.

Here is the detailed history and investigations of the patient:


BRIEF HISTORY OF THE PATIENT AND HIS PROBLEMS IN ORDER OF PRIORITY:
18 year old male presented with:
  1. Bilateral lower limb weakness since 1 month.Weakness in proximal and distal muscles.
  2. History of wasting and thinning of muscles.
  3. History of pain in the calf muscles while walking.
Weakness may be due to upper motor or lower motor neuron diseases.
PAST HISTORY:
Not a known case of DM/HTN/Epilepsy/CVA/CAD.
PERSONAL HISTORY:
Diet:mixed
Appetite:normal
Bowel and bladder movements:regular
History of alcohol consumption since 2 years:twice weekly
No history of smoking
FAMILY HISTORY:
No significant history.

NERVOUS SYSTEM EXAMINATION:
Higher mental functions-normal
Cranial nerves-intact
MOTOR SYSTEM: 

 RIGHT  LEFT
BULK decreaseddecreased
TONE:ULnormalnormal
       LLhypotoniahypotonia
POWER:UL 4/54/5 
            LL3/53/5
Deep tendon reflexes:  
 Bicepspresentabsent 
 Tricepsabsentabsent 
 Supinatorabsentabsent
 Kneeabsent absent
 Ankleabsent absent

SENSORY SYSTEM:normal
CEREBELLUM:normal

ANATOMICAL LOCALIZATION OF SITE OF LESION:
No upper motor neuron lesion signs are seen like spasticity,clonus,hyperreflexia,hypertonia and extensor plantar response.Therefore UMN lesion can be ruled out.
Hypotonia,absent deep tendon reflexes,muscle wasting suggest a lower motor neuron lesion.
SITES OF LOWER MOTOR NEURON LESION:
  1. ANTERIOR HORN CELL
  2. SPINAL NERVE ROOT AND PLEXUS
  3. PERIPHERAL NERVE
  4. NEUROMUSCULAR JUNCTION
  5. MUSCLE
AHC lesions,radiculopathies and plexopathies often present asymmetrically.
NMJ problems show typical fatiguability,fluctuating weakness and ocular/pharyngeal musle involvement.
Myopathies are pure motor lesions,they also have a symmetrical muscle invovement but reflexes are intact.
Thus it is clear that the lesion is in the peripheral nerves.

ETIOLOGICAL DIAGNOSIS:
Peripheral polyneuropathies can be axonal or demyelinating.
Nerve conduction studies help in identifying the type of neuropathy.
  AXONAL  DEMYELINATING
 MOTOR NCS:
CMAP		 decreased normal
Distal latency normal prolonged
Conduction velocity  normal slow
Conduction blocks absent present
F wave and H reflex  normal/absent prolonged/absent

NCS of the patient revealed bilateral common peroneal and sural axonal neuropathy.

CAUSES OF AXONAL NEUROPATHY:
  • Alcoholism
  • Diabetes mellitus 
  • Hypothyroidism
  • Vitamin deficiencies(B1,B12,E)
  • Drugs(isoniazid,pyridoxine,phenytoinchloroquine,certain anticancer drugs)
  • Hereditary motor sensory neuropathy(CMTD type 2)
KEY INVESTIGATION FINDINGS:
  • Perpheral blood smear was normal:no evidence of megaloblastic anemia(VIT-B12 deficiency)
  • Thyroid profile:T3 levels-mild decrease,TSH-normal
  • HIV serology:negative
Chronic alcohol consumption causes painful peripheral neuropathy.Associated nutritional deficiencies and direct toxic effect of alcohol results in alcoholic neuropathy.

PATHOPHYSIOLOGY OF ALCOHOLIC POLYNEUROPATHY:
  • Acetaldehyde is toxic to peripheral nerves.
  • Thiamine deficiency is common in chronic alcoholics.Cells cannot maintain the levels of ATP in the absence of thiamine.

Effects of alcohol depend on:frequency of drinking,quantity consumed,age of onset of drinking,duration of drinking,gender and genetic factors.

FURTHER INVESTIGATIONS:
  • Sural nerve biopsy is planned 
TREATMENT OPTIONS:
  • VITAMIN B COMPLEX SUPPLEMENTATION
  • Physiotherapy
  • Management of calf pain
My  references:-

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