A case of Bilateral venous thalamic infarcts

An Interesting Case of

Drowsiness

Dr.Arul Selvan Unit

Dr.Safinaaz UnitPresenter: Dr.M.Ramesh Babu

Brief HistoryMrs. X 49yrs old woman house wife basically from

Assam, settled in Chennai without any comorbids

presented with ℅

Fever 3 days , vomiting 3 days, sudden

unresponsiveness 1 day , Mild headache - 3 weeks.

On the day 13.10.2017 morning she felt uneasy, not

interested in doing house hold work - took cup of

coffee and slept @ 11 am - found unresponsiveness

on the bed - noticed by daughter @ 4pm - no witness

of seizures - regained consciousness in ambulance

and brought to ER @8pm.

H/o fever with polyarthralgia - since 3 weeks , treated

with steroids and hydroxychloroquine ( stopped 4

days back)

h/o Chronic migraine + , No h/o seizures/ tongue bite/

diplopia/ dysarthria/dysphagia/ weakness in any of

the limb, no h/o imbalance while walking , Urinary

incontinence +

No h/o weight loss/ night sweats/ past h/o

Tuberculosis

No h/o similar complaints in the past

No h/o any drug intake (OC pills) /sedatives /

exposure to pesticides

H/o ayurvedic medicine and green coffee usage +

Travel history to Mumbai - in Sep. 1 st. week.

No h/o recent vaccination

Family History - Nil significant

Obstretic history - nil significant

History Summary

49yrs old woman with chronic migraine presented

with fever , vomiting and sudden unresponsiveness

for 3 days without any comorbids on the background

of Viral polyarthitis on steroids and

hydroxychloroquine without seizures/skin rash/ weight

loss/ drug intake/ normal obstetric history.

Probable diagnosis: Acute Encephalitic syndrome ?

viral ? vascular ? metabolic ? toxic

On Clinical ExaminationShe is moderately built and nourished,

No pallor/ icterus/ cyanosis/ clubbing/

lymphadenopathy/ pedal oedema / no skin rashes/ no

thyoromegaly

Vitals : Temp- N, PR- 78/min, BP 160/90mmhg

CNS - Examination :

Patient is drowsy GCS- E2V1M3 , Pupils 2.5mm B/l

reactive, eyes midline, OCR+ , Fundus - Normal,

Moves all 4 limbs, DTR’S - sluggish, Plantar - B/L

Extensor, Neck supple

InvestigationsHB- 10.5 gm%

TC- 8100, PCV- 35, Platelets- 2.84 lakhs, DC- P-58 L-

31,E-6,M-5, ESR-89 mm/hr , CRP-8.2 (<5.0)

Sodium- 137 mmol/l, K+ - 4.8 mmol/l, S.Ca+ - 8.9 , RFT-

Normal, LFT- Normal , TSH- 1.4 miu/ml

CSF- TC- 5 cells ( all lymphocytes) , RBC- 150 , protein -

124 mg/dl,Glucose- 69 mg/dl, Cl- 121 meq/l, gram stain -

occ. pus cells, fungal stain - neg, AFB- Neg, Xpert TB-

neg, Blood for c/s & CSF c/s - neg.

Meaningoencephalitis panel - Neg.

U/S abdomen - B/L pleural effusion with bulky uterus.

MRI/MRA/MRV

MRV

MRA

Anti phospholipid IgM&G - Neg , Anticardiolipin Ab -

Neg, Lupus Anticoagulant- Neg,

Thrombophilia work up - negative, Protien C&S- Neg,

Factor V - Prothrombin gene mutation- Neg, JAK2

V6- Neg.

Vasculitis panel ANCA , ANA, dsDNA , MPO & PR3 -

negative

S. Homocysteine - 11.72 (<12), S.Ferritin - 10.7

(10.0-120.0), D-Dimer - 5.14(<0.5)

MTHFR Mutation - C677T Heterozygous Detected

Patient started on Heparin - and other supportive

medications.

On 15.10.2017 patient is more drowsy and developed

paucity of Rt upper limb with deviation angle of mouth

to left side.

Repeat MRI done

Final Diagnosis

CVT - B/L Venous Thalamic infarcts ? cause MTHFR

v6 mutation ? Steroids

Treated with anticoagulants - Recovered well and

discharged.

DD’s to a patient with B/L Thalamic

hyperinsentive lesions

• vascular

◦ deep vein occlusion: internal cerebral veins, vein of Galen, or straight sinus

◦ arterial ischemia

▪ artery of Percheron occlusion

▪ top of the basilar artery syndrome

◦ vasculitis

• hypoxic-ischemic encephalopathy

◦ infection/inflammation

◦ acute disseminated encephalomyelitis

• Creutzfeldt-Jakob disease

• viral encephalitis JE, West Nile

• toxic/metabolic

◦ osmotic extrapontine demyelination

◦ Wernicke encephalopathy

• status epilepticus

• ilicit drugs

• inherited disorders

◦ mitochondrial disorders

◦ Wilson disease

◦ Fabry disease

◦ Fahr disease

• neoplasms

Methionine Cycle

Case 2

Clinical sign

Vertical gaze palsy

Video

Images

Clinico Radiological

mismatchThalamic lesion can produce the vertical gaze palsy

by interrupting supranuclear inputs.

The mechanism for complete vertical gaze paresis

with thalamic lesions can be due to involvement some

of the frontocortical fibers which may decussate in the

medial thalamus. (can be seen in U/L lesion also)

Lesion of Supranuclear oculomotor

pathwaysBased on anatomical location:

Lesions of internuclear system

Immediate premotor structure in the brain

PPRF

Posterior commisure

Rostral mesencephalon

Cerebral hemisphere

Descending pathway from cerebral hemisphere

Superior colliculus

Thalamus

Thalamus blood supply

Thank you