Mrs. X, a 49-year-old woman with chronic migraine, presented with fever, vomiting, and sudden unresponsiveness for 3 days without any other medical conditions. Her symptoms occurred while taking steroids and hydroxychloroquine for viral polyarthritis. MRI showed bilateral venous thalamic infarcts, likely caused by cerebral venous thrombosis exacerbated by an MTHFR gene mutation and steroid use. She was treated with anticoagulants and recovered fully before being discharged.

1. An Interesting Case of
Drowsiness
Dr.Arul Selvan Unit
Dr.Safinaaz Unit
Presenter: Dr.M.Ramesh Babu

2. Brief History
Mrs. 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.

3. 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 +

4. Travel history to Mumbai - in Sep. 1 st. week.
No h/o recent vaccination
Family History - Nil significant
Obstretic history - nil significant

5. 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

6. On Clinical Examination
She 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

7. Investigations
HB- 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.

8. MRI/MRA/MRV

10. MRV

12. MRA

14. 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

15. 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

19. Final Diagnosis
CVT - B/L Venous Thalamic infarcts ? cause MTHFR
v6 mutation ? Steroids
Treated with anticoagulants - Recovered well and
discharged.

20. 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

21. Methionine Cycle

23. Case 2

24. Clinical sign
Vertical gaze palsy

25. Video

27. Images

29. 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)

30. Lesion of Supranuclear oculomotor
pathways
Based 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

31. Thalamus blood supply

32. Thank you