HEMIPARESIS
I've been given these three cases data here (https://medicinedepartment.blogspot.com/2020/05/three-patients-of-hemiparesis-case.html?m=1) to solve in an attempt to understand the topic of “Hemiparesis”
In case 1,
The complaints of the patient are :
- Headache which was intermittent, throbbing type, diffuse, bilateral since 2 years
- Knee joint pain and elbow joint pain since 6 months not associated with restriction of joint movement or morning stiffness.
- Multiple body pains, Disturbed sleep, Auditory hallucinations, Double vision.
She was referred to psychiatrist opinion and was diagnosed with severe depression and anxiety without psychosis - stressor factor being death of her younger son.
She was put on antidepressants and anti anxiety drugs for a week.
- The patient started swaying on either side and weakness of right upper and lower limb.
- She fell down and there was sudden development of loss of speech for 6-8 hours.
CT brain showed an old calcified granuloma in left high parietal region - which wasn’t significant.
MRI showed acute infarcts in bilateral capsuloganglionic region and left cerebellar hemisphere.
The infarct caused must have been the reason for her symptoms.
The infarct caused must have been the reason for her symptoms.
Anti platelets, Statins were given.
Routine investigations didn’t show any abnormalities.
Inspite of medications the symptoms were not relieved.
In addition she added
Routine investigations didn’t show any abnormalities.
Inspite of medications the symptoms were not relieved.
In addition she added
- Continuous giddiness more while walking but was comfortable lying down
- Intermittent horizontal binocular Diplopia
- Increased weakness of right upper and lower limbs
On examination,
The head is turned towards right and left eye is closed.
Deviation of mouth towards left and loss of nasolabial fold
3rd cranial nerve was abnormal - Right elevation, depression, dextroelevation, dextrodepression.
6th cranial nerve - Mild restricted abduction
Patient is unable to hold air in the cheeks, but able to whistle
Hypotonia in right lower limb
Reduced power in right lower and slight reduction in upper limb.
Ataxic gait
Progressive weakness of right upper and lower limbs with intermittent headache, bilateral pyramidal sign, left UMN facial paresis, 3rd and 6th cranial nerve palsies, cerebellar involvement is found.
From these the etiology may be stroke or a demyelinating disorder or basilar artery occlusion.
For further evaluation, MRI With angiogram was done
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| T2 hyperintensities along short segment of spinal cord |
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| T2 flair showing hyperintensity right internal capsule |
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| T2 flair showing hyperintensities in midbrain and bilateral thalami |
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| T2 weighed transverse section MRI showing hyperintensity involvement of midbrain sparing red nucleus. |
Carotid artery Doppler showed a soft plaque with smooth surface without any calcification or ulceration in the left.
Echo and ECG were normal.
Lumbar puncture showed high protein with lymphocyte predominance.
This is suggestive of a inflammatory process.
Based on the above history, clinical findings and investigations,
A differential diagnosis of Neurobehcets and Neurosarcoidosis was made.
NEUROSARCOIDOSIS :
Neurosarcoidosis generally occurs only in cases of sarcoidosis with substantial systemic involvement, and signs of neurologic involvement usually are seen in patients known to have active disease. Strictly neurologic forms are seen in fewer than 10% of patients; a subset has predominantly neuromuscular involvement.
Active sarcoidosis results from an exaggerated cellular immune response to either foreign or self-antigens. T-helper lymphocytes proliferate, resulting in an exaggerated response.
Three hypotheses have been proposed to explain the mechanism, as follows:
- A persistent antigen (either foreign or self) triggers the T-helper cell response.
- Response of the suppressor arm of the immune response is inadequate and cannot prevent T-helper cells from shutting down.
- A possible inherited or acquired (genetic) difference in response genes leads to the exaggerated response.
TREATMENT :
Immunosuppression is the principal method of controlling the disease, and corticosteroids are the cornerstone of therapy. In cases of exacerbation, intravenous pulsed methylprednisolone followed by oral taper may be necessary. Treatment is guided by the clinical response to corticosteroids. If the response is favorable (ie, steady amelioration of symptoms), then the dose may be tapered over several months. Follow-up by a neurologist every 3-6 months to monitor the progress of the disease is important.
(Source-Medscape)
A chest X-ray was done
There are a few reported cases of isolated neurosarcoidosis.
NEURO-BEHCETS:
This shows only few percent of people show Neurologic symptoms prior to systemic manifestations, and most commonly they develop within 6months - 1 year ,( range 6 months -3years )
On the other hand, Ikedat7 stressed that the common neurologic features of neuro- Behqet's syndrome were motor impairment especially bilateral pyramidal signs and that the mental changes mainly consisted of loss of emotional control with relative sparing of intelligence and memory.
On treatment with Methyl Prednisolone IV the patient is improved symptomatically and objectively power was improved in upper limbs and lower limbs over a period of 2 to 3 days.
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In case 2,
The complaints of the patient are,
- 3 episodes of vomitings 6 days back followed by altered sensorium.
- Intermittent headache
The patient was admitted in our ICU with high grade fever spikes and severe leucocytosis suggestive of sepsis along with a mass lesion and hematoma and she was empirically managed with IV antibiotics and her fever spikes and leucocytosis recovered.
Her coma took a few more days to recover spontaneously and she was finally able to mobilize herself with persistent neurological deficits.
She still has mutism due to an affection of the Broca's area (insert into the diagnosis) and possible other cognitive deficits yet to be ascertained.
The patient is Responding only at times
Lying on bed unable to move her right arm and leg
Not uttering words but responding to sounds at times non verbal communication at times though a bit slow.
On examination,
Pallor, mild dehydration, malnutrition are present.
The patient was unconscious, stuporous, no response to speech
A few cranial nerves were elicited and found normal.
Increased plantar reflex on right side and withdrawal on left.
MRI showed capsuloganglionic hemorrhage.
Diagnosis of CerebroVascularAccident with Right sided hemiplegia, Acute haemorrhage involving left Corona Radiata and Lentiform nucleus, Internal capsule with intraventricular extension was made.
HEMORRHAGIC STROKE:
In intracerebral hemorrhage, bleeding occurs directly into the brain parenchyma. The usual mechanism is thought to be leakage from small intracerebral arteries damaged by chronic hypertension. Other mechanisms include bleeding diatheses, iatrogenic anticoagulation, cerebral amyloidosis, and cocaine abuse.
Intracerebral hemorrhage has a predilection for certain sites in the brain, including the thalamus, putamen, cerebellum, and brainstem. In addition to the area of the brain injured by the hemorrhage, the surrounding brain can be damaged by pressure produced by the mass effect of the hematoma. A general increase in intracranial pressure may occur.
Causes of hemorrhagic stroke include the following:
- Hypertension
- Cerebral amyloidosis
- Coagulopathies
- Anticoagulant therapy
- Thrombolytic therapy
- Arteriovenous malformation, Aneurysms, and other Vascular malformations
- Vasculitis
- Intracranial neoplasm
TREATMENT:
Amikacin, Ceftriaxone, Ofloxacin - antibiotic
Paracetamol
Fluoxetin - SSRI
Donepezil and memantine - DONAMEM - Cholinesterase inhibitor
Air bed with frequent change of position.
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In case 3,
The complaints of the patient are
- Intermittent, low grade fever since 2 days
- Loose stools since 2 days - 10 episodes/day
- 1episode of non bilious vomiting
- Decreased urine output since 2 days
- Facial puffiness since 1 day
- Right upper limb and lower limb weakness with slurring of speech since october 2019 (Hemiparesis secondary to infarct in the Right parietal region)and is on regular anti-platelets.
- HTN since 8 months and is on regular medication (T.olmesartan+T.hydrochlorthiazide)
The blood pressure was 50/20 mm hg at the time of presentation
With this presentation she was immediately resuscitated with IV Fluids, NS at 20ml/kg bolus, later the on examination it increased to 80/50mmHg
Based on the complaints, kidney failure was suspected and RFT was done.
Abnormal RFT and LFT findings were present.7
Micro cystic hyper chronic anemia was found.
From the above examination and investigations, a diagnosis of ACUTE KIDNEY INJURY secondary to acute gastroenteritis was made.
It is also associated with hypovolemic shock, metabolic acidosis and anemia.
ACUTE KIDNEY INJURY FOLLOWING GASTEROENTERITIS:
Acute gastroenteritis resultS in different combinations of diarrhoea with vomiting, fever and abdominal pain.
Acute kidney injury is rapid deterioration in renal function resulting in accumulation of metabolic waste, sufficient to cause uraemia, following variety of insults to previously normal kidneys.
Several factors affect prognosis of acute kidney injury like oliguria, a rise in serum creatinine greater than 3 mg%, older debilitated patients, multi organ failure, associated co-morbid conditions, need for dialysis, suspected or proven sepsis.
The auto regulatory response normally renders an individual relatively resistant to prerenal forms of acute renal failure; however, a marked decrease in renal perfusion pressure below the auto regulatory range can lead to an abrupt decrease in GFR and lead to acute kidney injury.
TREATMENT:
Odansetron - ZOFER an antiemetic
Sporolac for diarrhoea
Plenty of oral fluids 2 L/day to recover the loses
Soft oral diet.
ORS
Sodium bicarbonate - NODOSIS to treat metabolic acidosis and diarrhoea
Blood transfusion for anemia.
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