Mr. L, a 37-year-old Native American man with alcohol abuse disorder presented to the emergency room with sub-acute development over two days of ataxia, bilateral lower extremity paralysis and loss of sensation below the nipple line. Five days prior, the patient began to feel lethargic and confused. His symptoms progressed to include significant lower extremity weakness, ataxia and loss of bladder control. In the emergency room, he received a new diagnosis of HIV.
At presentation, his vital signs were normal. He had intact strength and reflexes in upper extremities bilaterally and 0/5 strength and 1+ reflexes in lower extremities bilaterally. He had loss of all sensation below dermatomal level T4. On the third day of hospitalization, he developed non-reactive, anisocoric but accommodating pupils. Cerebrospinal fluid analysis is detailed in Table 1 and was positive for several infections including neurosyphilis (+VDRL), cytomegalovirus (+DNA), varicella zoster virus (+DNA), Lyme disease (+antibody) and Epstein-Barr virus (+DNA). Interestingly, none of these infections were detected in the serum. Serum HIV viral load was 52,379/mL, with a CD4 count of 21. Magnetic resonance imaging showed T2 FLAIR hyperintense lesions throughout the gray matter of the brain and diffuse T2 hyper-intense signal within the thoracic spine. He was treated with 14-day course of intravenous Penicillin for neurosyphilis and a 21-day course of Ganciclovir and Foscarnet for CMV, VZV and EBV. Soon after, he was also started on highly active anti-retroviral therapy and long-term Sulfamethoxazole/Trimethoprim, Azithromycin and Valganciclovir for Toxoplasmosis, Mycobacterium avium and CMV prophylaxis, respectively. A week into his hospitalization, he developed seizures which were controlled with Levetiracetam and Phenytoin. At hospital day 67, Mr. L had regained minimal motor and sensory function in the distal lower extremities and was discharged to a long-term skilled nursing home, with ambulation restricted to wheel chair use.
Discussion: This case represents an unusual presentation of a patient sub-acutely developing significant neurological deficits and subsequently being diagnosed with five concurrent CNS compartmentalized diseases, secondary to previously unknown AIDS. Though the patient’s presentation and progression of disease suggests the most likely cause to be CMV polyradiculopathy, it is important to treat all infections as 15% of such cases can be due to multi-organism disease.
Conclusions: AIDS can present in many different ways. An extensive work up of patients with unusual neurological presentations, along with targeted but thorough treatments are critical to prevent serious sequelae secondary to AIDS and associated invasive infections.