Three cases of paraparesis
I've been given these 3 cases to solve in an attempt to understand the topic of "patient’s clinical data analysis" to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and come up with a diagnosis and treatment plan.
CASE : 1
You can find the entire real patient clinical problem in this link here..
CASE : 1
You can find the entire real patient clinical problem in this link here..
Following is my analysis of this patient problems
Chief complaints are -
1. Weakness of bilateral lower limbs since 5 days with tingling & numbness
2. Vomiting 5 days back 3-4 episodes, non-projectile, non-bilious, food particles as content
3. Gluteal abscess since 5 months
4. Scrotal abscess since 20 days
WEAKNESS OF LOWER LIMBS
- Sudden onset , 5 days ago , associated with tingling & numbness , h/o sudden fall when got up for urination
This weakness can be attributed to either vascular / neural / muscular causes. To know which is causing let’s analyse
a) Vascular cause - There is h/o sudden fall which may be indication of vascular cause (in brain like ischemia , infarcts etc., or can be PVD ) . Here in this case there are no signs pertaining to the PVD (like varicosities , Claudication , atrophy etc.,) so it can be ruled out. But to know the brain involvement we should do an MRI
b) Neural cause - Weakness can also arise due to any nervous system abnormality and to rule out we must have a thorough examination of the patient regarding nervous system which is given below
c) Muscular cause - Weakness can be due to myopathies but there are no evidence of it...
The following are the results of nervous system examination;
Cns conscious
speech-normal
cranial nerves intact.
MOTOR SYSTEM
Right. Left
Bulk: normal. Normal
Tone: ul. normal. Normal
LL. hypotonia hypotonia
Power rt. lt
ul. 5/5. 5/5
LL. 2/5. 0/5
Reflexes.
Superficial reflexes
Right. Left
Corneal. P P
Conjunctival P. P
Abdominal. P. P
Plantar Extensor Extensor
Deep tendon reflexes
Right. Left
Biceps. 2+ 1+
Triceps. 2+ 1+
Supinator. 3+ 2+
Knee 3+ 2+
Ankle. 3+ 2+
jaw jerk. 1+. 1+
ankle clonus present. absent
Primitive reflex -absent
Involuntary movements - absent
SENSORY SYSTEM - normal
CEREBELLUM
titubation - absent
Nystagmus- absent
Intensional tremors - absent
Pendular knee jerk - absent
Coordination test -normal
MENINGIAL SIGNS
Neck stiffness - negative
Kernigns sign - negative
Brudzinkis sign - negative.
From the above results, we can see that as cranial nerves are intact we can rule out brain stem involvement, sensory system is normal, it could be UMN or LMN. As most of the features are suggestive of UMN, we can rule out LMN. It could be anywhere from cortex to anterior horn cell.
Investigations done are MRI & X-ray which showed the following;
- There are significant enhancement representing meningeal enhancement or exudates
- Multiple nodules in pulmonary spices suggesting Pulmonary Kochs and disseminated TB.
From MRI we can see that it is an UMN lesion, but to know where exactly we should know about motor hormonculus.
we all know that the motor functions of the body are controlled by the Primary Motor Cortex area in the frontal lobe along the precentral gyrus....
And there neurological map dedicated to motor functions of different body parts called MOTOR HOMUNCULUS in the primary motor cortex area...
Since our patient had weakness of legs there should be lesion at the leg area of the Motor Homunculus.
Let’s see where the leg area is present.
So the leg area will be in the medial side of the each hemisphere corresponding to the longitudinal groove where the falx cerebi descends down vertically....
Here in the patient the MRI features are also seen at the same regions....so we got the exact location of the UMN lesion...
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.
Possible diagnosis : Dissemination of TB to the brain particularly to the falx cerebri region affecting the motor homunculus mainly the leg area causing weakness of the lower limbs....
Treatment given :
T.ATT 3 tabs/day fdc
T.Benadon 40mg/od
T.pregabalin 75mg/po/h/s
OINT.MEGAHEAL FOR LOCAL APPLICATION
SITZ BATH WITH BETADINE TID
FREQUENT CHANGE OF POSITION.
Case 2 :
You can find the entire real patient clinical problem in the below link :
Following is my analysis of the patient problems
1. Difficulty in walking since 1 month
2. Bilateral lower limb weakness since 1 month
3. Pain in lower limb calf muscles since 1 month
4. Fever since 1 week
DIFFICULTY IN WALKING & WEAKNESS IN LOWER LIMBS
It is of sudden onset since 1 month in the both legs below knee near the calf associated with difficulty in standing from sitting position, climbing stairs, holding chappals...
So this can be attributed to any abnormality in Muscle / Vascular / Nervous....let's analyse them..
a) Muscle related - if it is so there should be increased creatine kinase levels....but no evidence of it and no h/o muscle hypertrophy or wasting...so we can rule out this too..
b) Vascular related - there is no h/o varicosities, claudication , atrophy...so it can also be ruled out...
c) Nervous related - to know about this we must have a through nervous system examination...
Based on examination :
There is no sensory involvement, no involuntary movements, no cerebellar involvement.So I cut done my differential diagnosis to upper motor neuron lesion and lower motor neuron lesion.
Findings of examination show that there is atophy, hypotonia, absent deep tendon reflexes and babinski is neagative.
Based on this finding I confine my diagnosis to LMN lesion.Now problem arises where exactly is the site of lesion as LMN involves anterior horn cell,dorsal root ganglion, spinal nerve root , peripheral nerve, NMJ, and muscle.
The electromyography showed normal so NMJ involvement is ruled out...and we left with the peripheral nerve....to know that we have to do nerve conduction studies which showed that
“BILATERAL COMMON PERONEAL & SURAL AXONAL NEUROPATHY”
So from above it is evident that axonal degeneration is causing all his symptoms...
From the h/o the patient is alcoholic...so which can cause deficiency of vitamins B1,3,6 and lead to peripheral neuropathy. Due to these metabolic disturbances there can be accumulation of fructose and sorbitol in Schwann cell which can lead to axonal degeneration....But rule out other causes a Sural nerve biopsy is indicated and the results are awaited...
The other problems like pain & fever can also be attributed to this because of the inflammation in the nerves...
Pathological cause could be :
- Toxic : Alcohol
- Deficiency : Vitamin B12
Treatment received by this patient :
T.PCM 650mg/ TID
INJ.NEOMOL 100ml/ IV INFUSION IF TEMPERATURE >101F
TEMPERATURE CHARTING 4th HOURLY AND TEPID SPONGING
PERMETHRIN 5% LOTION OVERNIGHT APPLICATION ALL OVER BODY EXCEPT FACE (for scabies)
Additional treatment required:
-Complete abstinence from alcohol .
-For painful peripheral neuropathy- PREGABALIN may be helpful
-INJ. Vitamin B12 - twice weekly I.M. May be helpful for megalobalstic anemia.
-vitamin supplements ( folate ,B12, B6.)
Case 3 :
You can find the entire real patient clinical problem in the given link below :
Following is my analysis of this patient problems
Mainly he came with the chief complains of
1. Weakness of both lower limbs since 20 days
2. Bilateral edema of lower limbs
WEAKNESS OF LOWER LIMBS
It started in the proximal region initially 2yrs back which is insidious in onset & gradually progressed to distal region....It has been associated with the difficulty in wearing and holding chappals ...
So let’s analyse this weakness in lower limbs.....this can be attributed to either Vascular or Neural or Muscular system abnormalities!!!!
a) Vascular cause - Here we didn’t see any sign of PVD like varicosities , claudication , atrophy so it can be ruled out...
b) Neural cause - To know this we must have a thorough nervous system examination.....and the following are results....
patient is conscious, coherent, coperative
patient well oriented to time, place and person
higher mental functions= normal
Cranial nerves- intact
Motor system-
tone - normal
power - 4-/5 in both lower limbs
reflexes absent in both lower limbs
sensory system-normal
No meningeal signs
No cerebellar signs
From the above results....there is no evidence of hyper reflexes or spasticity....but there is absent of reflexes which leads us to think about the LMN involvement..
So it can be any where from the Anterior horn cell to the Neuromuscular junction....broadly at the peripheral nerve or at the NMJ...
-To know whether it is peripheral nerve related; we must do nerve conduction test which showed normal.
-To know whether it is NMJ related; we must do electromyography which again showed normal...
So the neural cause also ruled out,and we are left with muscular cause.
c) Muscular cause - To know this we have to examine creatine kinase levels & do muscle biopsy...
And the results came out as ; there is increased creatine kinase levels and biopsy of Quadriceps Femoris showed no evidence of polymyosis but suggestive of dystrophy...
- Dystrophies : it is more likely to be because there is proximal muscle weakness first and also the biopsy showed fat cells , necrotising and regenerative muscle fibre....
So what type of Dystrophy is causing this?..there are mostly 3 common types of dystrophies like Myotonic , Duchene’s , Becker’s....
- Myotonic dystrophy can be ruled out as it will starts with facial muscle weakness and mostly sparing proximal muscles
- Duchene’s Muscular dystrophy can be ruled out as it presents in the early life at 3 to 5 yrs & these persons usually wheelchair bound in adolescence or die in their late teens due to severe pulmonary infections
- So , Becker’s Muscular dystrophy is most likely to be the diagnosis....
Becker's Muscular dystrophy :
It is a X-linked recessive disease presenting at 5 to 15 yrs of age with weakness in the muscle due to reduced Dystrophin which is a protein connecting cytoskeleton of muscle to extra cellular membrane providing strength & stability to muscle. It presents with; muscle weakness , pseudo hypertrophy of calf muscles due to infiltration of fat cells , use of Gower’s manoeuvre to get up from floor.
Signs and symptoms:
muscle wasting
cardiomyopathy
arrythmias
scoliosis
features of myopathy
Investigations:
CK-MB
EMG
Muscle biopsy
Chest x-ray
genetic testing.
Therapeutic options :
- There is no specific cure for Becker’s muscular dystrophy.
-We may prescribe steroids to help the individual able to walk for as long as possible (as it increases the production of protein Utrophin a close resemble of Dystrophin).
- Physiotherapy may be helpful to maintain the strength if the muscle.
-There should be repeated monitoring of cardiac parameters because it is the main cause of mortality...
-Presently new strategies like Using stem cells for repairing damaged muscle fibres , Insertion of new Dystrophin genes etc., are being experimented...