This is a case of a 66 year old male, Known hypertensive and type II diabetes for the past 15 years (on medication, but poorly controlled). He presented at the A & E with complaints of mild left upper limb weakness & slurred speech which started simultanoeuslt half an hour earlier. There was no history of other limb weakness, sensory loss, LOC, headache, nausea or vomiting, diplopia,chest pain or palpitations. He had past history of a stroke in 2001 (quadriparesis) as well as a CABG done in 1996 following several episodes of chest pain.Besides 3 oral hypoglycemics, he was also on Aspirin, ARB,Digoxin, Simvastatin and Warfarin.
On admission, he was investigated, treated & monitored regularly. However on the next day, he complained of severe weakness of the left upper limb (totally could not move hand and digits) with no change in sensation. On the 3rd day his upper limb weakness regressed and so did the slurring of speech.
On examination (3rd day), he was concious,Orientated to time place & person, GCS was 15/15. Gait was normal. Vitals ; pulse of 78 Bpm; irregularly irregular with pulse apex deficit (atrial fibrillation; rate controlled); BP was 150/90 mmHg ; R/R : 20 / min ; and afebrile. JVP was not raised, both carotids palpable equally. There was a sternotomy scar on the chest & bilaterally stripped GSV graft scars (from medial malleolus to below knee).
On CNS examination, mild dysarthria noted; no nasal twang in speech (variable pitch & tone). Cranial nerves examination revealed left UMN facial palsy features (loss of left nasolabial fold, angle of mouth deviated to right, left buccinator weak) ; there was no diplopia, nystagmus or facial asthesia. Pupils were isocoric (4 mm) and reactive to light.Palate was normal, uvula central & gag reflex present. Tongue was deviated to the left side.
Motor examination - left upper limb spastic hemiplegia
Limb adducted, semiprone, hypertonia; Power was 4/5 in the arm, 3/5 in the forearm, 1/5 at the wrist 0/5 in the fingers.Triceps & biceps reflex was brisk, supinator jerk normal.No sensory or autonomic disturbances in the affected limb.
Both lower limbs had normal tone, grade 5 power, normal DTR and bilateral plantar flexion. No cerebellar signs.
On CVS examination:laterally displaced & diffuse apical impulse (Left ventricular volume overload) - hyperkinetic; no left parasternal heave normal S1 & S2 , no murmurs.
Impression : Left upper limb monoplegia and left UMN facial palsy caused by thrombotic stroke ; with underlying AF, IHD, Hypertension & diabetes.
Reasoning : In this case patient only has left upper limb weakness (purely motor) and UMN facial nerve palsy of left side which together can called as left Facio - Brachial monoplegia.The type of CVA is said to be thrombotic due to the presentation of progressive neurological deficit (increased weakness on day 2) . The common site of thrombosis in this case would be right corona radiata where minute thrombi cause lacunar infarcts (in region of fibres of arm & hand - brachial syndrome ). In some cases the facial weakness can be accompanied with non - confluent aphasia.
If the weakness of upper limb and face regresses within a 3 week interval this episode of CVA would be regarded as Reversible Ischemic Neurological Deficit and not a stroke.
The risk factor predisposing to a thrombotic stroke in this patient would be his age, underlying hypertension, diabetes, dyslipidemia, obesity sedentary life (retired), chronic smoking (past 30 yrs) and overwarfarinisation (on long term warfarin for AF - Clotting profile revealed INR of 1.3 ;too low)
However, we cannot deny the possibility of an embolic stroke (as well as recurrence) due to his underlying atrial fibrillation.
Thrombotic strokes
- middle ge & old
- Usually occurs during sleep ; patient gets up with weakness ; stroke
progresses over hours (stroke in evolution)
- Associated with past history of TIA
- Vomiting is absent, headache is mild or absent
- Meningeal irritation absent, convulsions rare
- Conjugate deviation of eyes absent, BP will be high
- CSF usually nomal
- Arterial thrombus forms due to underlying atherosclerosis of small and
medium vessels (lipohyalinosis) - hypertension, dyslipidemia, diabetes
etc.
- Also in arteritis, syphilis and collagen vascular diseases
- Cortical venous thrombosis/thrombophlebitis ; post partum or
postoperative (hypercoagulable states) - maintain INR between 2 & 3 with anticoagulants
- ICA thrombosis indicated by carotid bruit and absent pulse



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