Interesting Stroke Case
Prakash Balasubramaniam, M.B.
A 64 years man known to have HTN for 4 years, developed pain, numbness,
weakness of right LL for the past 6 months which is progressive for the past 2
months, aggravated on walking for more than 500 feet, during when he
gets tingling sensation in Right LL. There is history of fall 6 months ago
with a minor fracture in Right LL. There is H/O slurred speech for 3 months.
He used to smoke 2 pkt of cig/ day and occasionally used to consume alcohol.
Examination on day-1 ( 8/3/06) in OPD revealed normal power and
tone, sluggish reflexes, plantar – bilateral flexor without sensory
involvement or ataxia. After making him to walk for 10 mts he developed
paraesthesia of right LL along with diminished pinprick of entire right LL. KJ
became absent from sluggish. No other fresh deficits. SLR- negative. He
was diagnosed to have lumbar canal stenosis with Radiculopathy involving right
Basic Investigations did not reveal any abnormality. TSH is 0.894 micro
units/ml (0.27 to 4.2). He was on irregular treatment with Depin Retard 20mg
0-0-1, His pulse being 84, BP – 130/80 both lying, standing. At this
juncture, he was prescribed Gabapentin, Voltaflam, and Ranitidine.
Four days later he was admitted through EMD at 11 pm for the complaints of
right Hemiparesis which had started 6 hrs earlier. On further enquiry there is
history of swaying to right side on and off for the past 15 days. The weakness
was subacute onset and has progressed to some extent without any history of
vomiting, seizures, LOC. He never had such episodes earlier. Examination
revealed conscious patient with dense flaccid right hemiplegia, and motor
aphasia. He could comprehend well. He had facial weakness right hemianopia,
power being 2/5 in right sided limbs. Plantar extensor on right, systems NAD.
CT scan brain (within 10 hrs) showed small right paraventricular infarct
. His BP was 170/90 on admission.
ECG is normal, after checking APTT he was started on low molecular weight
heparin and antipalalets drugs along with antihypertensives. His MRI
showed bil paraventricular ischemic areas
On 3rd day of admission – His BP gradually increased from 150/80 (day
1) to 220/120 (day 3). His weakness remains same. He was alert, 2nd
antihypertensive drug was added. However the BP was further increased
(210/100) on 4th day and he required 3rd and 4th antihypertensive drug which
did not control the BP, the dose was further increased. Mean while
he became more drowsy, arousable with deep pain. No fresh neurological
deficits. He was found to have intermittent drowsiness with active gaze
deviation to left side for which EEG was done which showed poor background
alpha on left side, theta activity on both side left more than right
predominately on left fronto temporal region. He was started on
Carbamazepine 600mg/ day. On next day he was slightly more alert. BP was
reduced 160/90 and his 2nd MRI showed increasing paraventricular ischemic
areas. However the patient did not became fully alert.
On day 6 (18.3.06) he was more drowsy LP done which is normal. He
required 5th anti hypertensive drug as the BP continued to be 200/ 100.
Anti HTNves are - Nicardia Retard 10mg 1-0-1, Atenolol 50mg 1-0-1,
Losartan 50mg 1-0-0, Hydrochlorthiazide 12.5mg 1-0-0, Arkamine 0.1mg ½ -0-0.
The CSF values are normal. As a patient became more drowsy and there is no
motor convulsion the Zeptol was withdrawn. After 2 days, his BP was
fairly under control. However the drowiness controlled due to the presence of
slow relaxing of AJ and the clinically obscure encephalopathy. He was started
on steroids and Eltroxin empirically. The Alertness became better. The HR
which was around 96 was reduced to 60. On introducing Aten there is further
drop to 50, and on withholding the same it increased. He was receiving
vitamin supplementation also orally. He was off antiplatelets drugs for 3 days
due to GI bleed. His BP 140/90, pulse remains 64, the level of consciousness
same. He was apathetic, drowsy, easily arousable, comprehenses and expresses
in monosyllabus. A small dose of mannitol was introduced.
On 16th Admission day (28/3/06) he became very drowsy suddenly not responding
to calls, became alert, after 100ml of mannitol. His dolls was nomral,
PERTL, Saturation, pulse, BP. He moves left limbs well, the Mannitol was
increased,and a complete metabolic recheck was done - all were normal. C&V
Doppler was nomral. MRI showed progressive increase in paraventricular
ischemic areas, both left more than left. Low molecular weight
heparin was restarted after APTT. Hypertensive check since admission revealed
7 episodes of sudden brief drop in BP more than 20mm of Hg both systolic and
diastolic from the previous valve scattered over a periods of 15 days once in
2 to 3 days. One episode being 90/70 on 7th admission day lasted for one hour.
CT scan and all the 3 MRI scan were attached,
The points to be clarified in this case are
1. Was the presenting manifestation of LCS a TIA ?
2. The patient presented with acute dense flaccid right hemiplegia with
dysphasia. Why didn't the imaging reveal any dense infarct ?
3. Why is there a progressive rise in BP after a few days of admission
requiring 5 drugs for its control ?
4. Whether the infarcts are at MCA or at border zone area ?
5. Though the likely pathology from the MRI should be carotid occlusion,
the C&V Doppler being normal.How to explain?
6. Weather the gaze deviation being taken as seizures?
7. what is the reason for his drowsiness ?
8. How to proceed further in this case?
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(c) 2006 M.H. Rivner
April 3, 2006