Presenting History:
A 72 year old male with Past medical history presented with history of self-limiting, intermittent near daily pressure like Right Sided (frontotemporal region) headache radiating to left side, usually responding well to analgesics since 3 months. He has reported headache worsened in afternoon. Patient has reported to be more forgetful, worsening memory. Patient’s primary caretaker (Daughter) has reported behavior changes with increased agitation/irritability and found the slowness of thinking. Patient has denied any vomiting, vision changes, dizziness, or vertigo, weakness or sensory changes. There was no history of seizures nor recent abnormal movements. No personal or family history of cancer was reported. Patient has reported being a long-term former smoker.
Physical Examination:
At admission to a local hospital, the patient had stable vitals and normal gross physical examination. His systemic examination including neurological examination was normal.
Neurological Exam:
Mental Status: AA OX3
follow commands:
- clear speech
- no dysphasia
- Cranial Nerves:
- Pupils equal
- eyes midline w/o gaze
- preference
- face symmetric
- no gross visual field cuts
- hearing intact grossly
- Tongue is midline
Motor Exam:
- MAE AG and to resistance
- Sensory Exam:
- LT/PP and pain intact
Coordination Exam:
- no gross ataxic movements
- no dysmetria
Reflexes Exam:
- DTR 2+ symm throughout.
- Gait: steady gait, able to tandem
Investigation:
CT brain is notable for left subcortical well circumscribed hypodensity involving thalamic region, concerning intracranial mass with perilesional edema and mass effect and MLS. Neurosurgery consulted which deemed not urgent immediate neurosurgical intervention. MRI brain w/wo GAD ordered for further evaluation for lesion. Decadron ordered and Keppra initiated seizure prophylaxis. Possible surgical intervention/planning pending MRI. Patient admitted to Neuro ICU for further monitoring.
His blood workup was within the normal range except for a mild leukocytosis. Since he had no acute infectious etiology of symptoms, it was possibly a reactive and most likely due to recent administration of steroids. CT brain was notable for left thalamic and left basal ganglia low-attenuated mass with 3.7 cm anteroposterior diameter, 3.6 cm transverse diameter and 3.9 cm craniocaudal diameter. It had adjacent vasogenic edema and mass effect on the third ventricle with 7mm midline shift towards the right consistent with a malignancy primary versus metastatic etiology.
MRI Brain WO/W Contrast showed a mass in the left thalamus and basal ganglia region with a thick rim of peripheral enhancement as well as internal septal and amorphous areas of enhancement. The mass measured approximately 3.9 x 3.8 x 3.7 cm. The central portions of the mass showed heterogeneous hyperintense T2 signal suggesting internal complex cystic or necrotic components. There was significant surrounding vasogenic edema with mass effect upon the brain structures and left-to-right subfalcine shift.
No malignancy or metastasis was found on both CT chest and CT Abdomen apart from an incidental left liver lobe cyst. The patient had moderate to severe valvular aortic stenosis on echocardiography.
Differential considerations for these findings are broad. Findings are concerning for primary or metastatic malignancy, however other etiologies including abscess/infection, lymphoma, or other etiologies would present a similar appearance and cannot be excluded.
Histopathology The biopsy was sent for a pathology examination. Microscopic sections showed cellular aggregates and minute fragments of hypercellular glial tissues with mild to moderate cytologic atypia but no evidence of increased mitoses and cell necrosis. The findings were consistent with Anaplastic Astrocytoma (WHO Grade III). On immunohistochemical staining, 100% cells were positive for cytoplasmic GFAP (3+) and 2% cells were positive for nuclear Ki-67 (3+).
Diagnosis: WHO GRADE III Anaplastic Astrocytoma
Treatment
The patient was managed with gamma knife radiosurgery, chemotherapy with Temozolomide (TMZ), and targeted molecular therapy with Bevacizumab. The patient improved with remission of symptoms. No more behavioural changes were noted.
Follow up:
Follow up in the outpatient neurology clinic was continued for six months with complete improvement in patient neurological status.