1416 - Bugged by Weakness

Case Diagnosis: Necrotizing toxoplasma encephalitis with obstructive hydrocephalus and severe right hemiparesis in the setting of newly diagnosed HIV and hepatitis B.

Case Description: A 50-year-old female with hypertension presented with two weeks of right hemibody weakness and facial droop. Brain MRI demonstrated multifocal enhancing lesions with mass effect, initially concerning for neoplasm. Stereotactic biopsy confirmed necrotizing toxoplasma encephalitis, concurrent with new HIV diagnosis (CD4 19). Her course was complicated by progressive edema and midline shift requiring EVD placement. At inpatient rehabilitation admission, she exhibited profound right upper extremity paraplegia (0/5 throughout), residual right lower extremity weakness (hip flexion 4/5, ankle dorsiflexion 4/5), right facial droop, sensory loss, and impaired safety awareness. She required moderate to maximal assistance for transfers and ADLs. She engaged in intensive physical, occupational, and speech therapy while receiving IV Bactrim and Biktarvy.

Discussions: Over the course of rehabilitation, the patient demonstrated meaningful neurological and functional gains. By discharge, she achieved improved balance, independence with oral intake, and progress with transfers despite persistent right hemiparesis and cranial neuropathies. Notably her cognition, language, and motivation remained intact, facilitating engagement with therapies. This case highlights the challenges in managing functional recovery in patients with opportunistic CNS infections complicated by acute neurologic conditions as well as an uncommon cause of a seemingly common presentation.

Conclusions:

Necrotizing toxoplasma encephalitis is a rare and uncommon cause of stroke-like presentation, particularly in patients with previously undiagnosed HIV. This case underscores the importance of maintaining a broad differential for acute hemibody weakness and facial droop. Early recognition of atypical etiologies and timely initiation of rehabilitation can optimize functional recovery even in the setting of profound neurologic deficits.