Paraparesis case study -1
Case of a 23 year old male with paraparesis
Submitted by : Simran Dash
MBBS - IV | Roll number - 153
"I've been given this case data
here:
https://vaish7.blogspot.com/2020/05/medicine.html?m=1
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)
Age: 23 years
Chief complaints of the patient:
Ø Weakness in both lower limbs (Paraparesis)
Ø Gluteal abscess
Analysis:
I) Paraparesis:
ØOnset - Sudden
ØDuration - 5 days
ØProgression - Gradually progressive
Ø Associated complaints - Vomiting 5 days back (non-bilious and non-projectile)
Ø Tingling and numbness.
Ø There is no diurnal variation (rules out myasthenia gravis)
II) Gluteal abscess:
Ø Onset - Sudden
Ø Duration - 5 months
Ø Was operated
Also has a history of scrotal abscess
20 days back for which Incision and drainage was done 10 days back.
Past History:
Ø Has a history of multiple sexual partners.
Ø Did not get vaccinated recently (Influenza vaccine can cause GBS like syndrome)
From the history I am of the opinion
that it could be a motor neuron disease.
On examination:
Ø Hypotonia in both the Lower limbs.
Ø Power is also reduced in both the lower limbs. (RL - 2/5; LL - 0/5)
Ø Babinski’s sign is positive.
Ø Deep Tendon Reflexes are reduced.
Ø Sensory system - normal
Investigations done on this patient
are:
Ø CBP: normal
Ø CUE: normal
Ø MRI OF Brain: There is significant enhancement which represents meningeal enhancement or exudates
Ø Chest x ray: multiple nodules in pulmonary apices
Ø Serology for HIV, Hepatitis B: negative
So, from the above I am of the opinion that:
Anatomical location of the root cause could be in the Spinal cord because:
Ø Sudden in onset.
Ø More common.
Findings which are needed to confirm this can
be:
Ø Bowel and bladder movements because urinary incontinence can point towards a lesion in the spinal cord.
Ø Mass reflex should be tested. If mass reflex is present that indicates severe spinal cord disease.
Pathological cause for this problem could be:
Ø Vascular
Ø Compression
Ø Demyelination
Microbiological cause:
Ø Mycobacterium tuberculosis
Ø HIV (because he has multiple sexual partners)
Ø Treponema pallidum
Biochemical cause:
Ø Defect in the gene “chromosome 9 open reading frame 72,” or C9ORF72 (seen in ALS)
Possible differential diagnoses could
be:
Acute Transverse myelitis
ALS (Amyotrophic Lateral Sclerosis)
Post vaccinial (ruled out from history already)
Arachnoiditis:
· TB spine (because Elevated Alkaline phosphatase points towards a problem in the bone, psoas abscess, Intracranial space occupying lesions and meningeal enhancement in MRI, and multiple modules in pulmonary Apices)
· Tabes Dorsalis (neurosyphilis)
Thrombosis of anterior spinal artery (myelomalacia)
Ø Lathyrism (can be ruled out from
family history)
ØSubacute combined degeneration of Spinal cord
Ø Alcoholic liver disease (because
there is elevated SGOT, and sensations of tingling and numbness)
Additional investigations required
are:
Ø Mantoux test: positive in TB
Ø Lymph node biopsy
Ø Lumbar puncture and CSF Analysis (for features of Froin’s loculation syndrome)
Ø Serum vitamin B12 levels
Ø Electromyography (muscles will be
affected in motor neuron disease)
Ø Nerve conduction study (to differentiate between motor neuron disease and peripheral neuropathy)
Ø VDRL test for syphilis
Ø Pupillary reflexes to be tested (Argyll Robertson pupil in Tabes dorsalis)
Ø Gait should be tested (tabetic gait characteristic of tabes dorsalis)
Ø Genetic testing for ALS
Treatment received by him:
Ø ATT 3 tabs/day fdc
Ø T.Benadon 40mg/od
Ø T.pregabalin 75mg/po/h/s
Ø Oint.megaheal for local application
Ø Sitz bath with betadine tid (For the gluteal abscess)
ØFrequent change of position
Additional treatments required are:
In caries spine:
·
Application
of traction in early stage.
·
Later
on, “plastic jacket” is applied for immobilization.
Ø Physiotherapy:
·
Passive
movements are carried out in the lower limbs once or twice daily.
·
Later
on, arrangement of wheel chair, walking calipers are done according to the
necessity.
Ø Surgery:
·
Drainage
of cold abscess
·
Laminectomy
for caries spine.
REFERENCES:
- https://pubmed.ncbi.nlm.nih.gov/31232571/
- https://en.wikipedia.org/wiki/Pott_disease
- https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Motor-Neuron-Diseases-Fact-Sheet
- https://www.medscape.com/answers/1169231-113721/what-is-tabes-dorsalis
- Clinical methods of medicine by Arup kumar Kundu
- Hutchison’s clinical methods
- Davisdson's principles and practive of Medicine
- Harrison's principles of internal medicine
"[5/22, 4:12 PM] Rakesh Biswas:
ReplyDelete"Anatomical location of the root cause could be in the Spinal cord?"
Where is the exact level in the spinal cord? Is it in the cervical, thoracic or lumbosacral segments? 🤔
[5/22, 4:19 PM] 2016 Kims: Lumbosacral segments sir
[5/22, 4:21 PM] 2016 Kims: But it could be lower thoracic and upper lumbar sir.
[5/22, 4:23 PM] 2016 Kims: I think we need more Data to confirm it sir. MRI spine should also be done
[5/22, 4:23 PM] Rakesh Biswas: What if I told you that the patient's upper limb reflexes were elicitable by me by just tapping with my fingers and even his biceps was jumping bilaterally
[5/22, 4:25 PM] 2016 Kims: Then it could be a upper motor neuron lesion sir. If it’s exaggerated then maybe it could be a UMN lesion
[5/22, 4:26 PM] 2016 Kims: His babinski sign is also positive
[5/22, 4:27 PM] 2016 Kims: But since he has hypotonia I thought it couldn’t be UMN
[5/22, 4:39 PM] Rakesh Biswas: In the stage of acute neuronal shock one can still have hypotonia in UMN
[5/22, 4:40 PM] 2016 Kims: Yes sir so how do we know that it a stage of acute neuronal shock?
[5/22, 4:49 PM] Rakesh Biswas: If the UMN findings such as hyperreflexia predominate you think of UMN with hypotonia due to acute neuronal shock.
If LMN findings such as areflexia predominates you think of hypotonia due to LMN
[5/22, 4:50 PM] 2016 Kims: Okay sir.
Thank you. So this could be a state of UMN lesion with hypotonia due to acute neuronal shock
[5/22, 4:51 PM] Rakesh Biswas: Yes and where is the UMN lesion located?
[5/22, 4:53 PM] 2016 Kims: I think it’s above the anterior horn cell in spinal cord
[5/22, 4:55 PM] 2016 Kims: Sir in the video you said it could be parasagittal meningioma but then the lesion should be in cerebral cortex for that
[5/22, 4:55 PM] 2016 Kims: And he does not have any features suggestive of cortical lesion like aphasia
[5/22, 4:56 PM] Rakesh Biswas: Where are anterior horn cells in spinal cord? 😅
[5/22, 4:57 PM] Rakesh Biswas: Are the areas of aphasia located all over the cortex? Is the leg area same as the speech area? 😅
[5/22, 4:58 PM] Rakesh Biswas: You will find anterior horn cells at every section you take of the spinal cord
[5/22, 4:58 PM] 2016 Kims: Oh yes sir. Sorry sir 😅
[5/22, 4:58 PM] 2016 Kims: I think the lesion is at the level of lower thoracic and upper lumbar vertebrae
[5/22, 4:59 PM] 2016 Kims: No sir. 😅
[5/22, 4:59 PM] 2016 Kims: It’s speech areas are brocas and wernickes
[5/22, 5:00 PM] 2016 Kims: So it could be parasaggital meningioma then?
[5/22, 5:06 PM] Rakesh Biswas: What about this then? 👆
[5/22, 5:08 PM] Rakesh Biswas: How do you explain the gluteal abscess and the mei report mentioning other things in that vertebral region?
[5/22, 5:13 PM] 2016 Kims: Sir i think that is a cold abscess.
Yeah then lesion is in lumbosacral region sir that could explain the abscess.
[5/22, 5:39 PM] Rakesh Biswas: So is the vertebral lesion producing any neurological signs?
[5/22, 7:07 PM] 2016 Kims: Yes sir I think it’s compressing upon the cord and causing the upper motor neuron signs i.e. hypotonia and exaggeration of reflexes
[5/22, 7:08 PM] 2016 Kims: Sir should I change it in my blog then ? That the reflexes are exaggerated
[5/22, 7:46 PM] Rakesh Biswas: Yes instead of deleting the previous you can add this as an edit
[5/22, 7:47 PM] Rakesh Biswas: But then where in the cord will the compression produce the paraparesis he is having?
[5/22, 8:03 PM] 2016 Kims: Okay sir. I will do that
[5/22, 8:04 PM] 2016 Kims: Sir because psoas muscle is supplied by L2,L3,L4 nerve roots so maybe the compression is over there
[5/22, 8:22 PM] Rakesh Biswas: So if the nerve root is compressed what will it look like? UMN or LMN?
[5/22, 9:02 PM] 2016 Kims: LMN sir
[5/22, 9:04 PM] Rakesh Biswas: And what are the dominant clinical signs in your patient suggestive of?
[5/22, 9:36 PM] Kims: So if the nerve root is compressed what will it look like? UMN or LMN?
[5/22, 9:36 PM] 2016 Kims: LMN sir
[5/22, 10:10 PM] Rakesh Biswas: So then the nerve root is spared ?"