Rapid onset of neurological symptoms in an HIV-positive patient with progressive multifocal leukoencephalopathy: a case report.

INTRODUCTION AND IMPORTANCE

Progressive multifocal leukoencephalopathy (PML) is a rare demyelinating disease of the central nervous system caused by substantial damage to oligodendrocytes. It clinically presents as movement impairment, cognitive disability, language aphasia, dysarthria, and visual impairments. It was first identified in 1958. It is commonly associated with either Hodgkin's lymphoma or chronic lymphocytic leukemia.

CASE PRESENTATION

A 40-year-old male Asian farmer presented with altered behavior, fever, and weakness on the right side of his body after suffering a widespread tonic-clonic seizure. His medical background included a tonsillectomy, treatment for pulmonary tuberculosis, and hepatitis C (negative polymerase chain reaction). On admission, he had asymmetric plantar responses, pallor, brisk deep tendon reflexes, an oral thrush, and decreased strength and tone in the muscles on his right side. The findings of the laboratory tests revealed elevated pH, red blood cells, lymphocytes, and protein in the cerebrospinal fluid, as well as an elevated erythrocyte sedimentation rate, abnormal liver function tests, and no bacterial growth. Magnetic resonance imaging (MRI) showed bilateral parietal, temporal, and frontal lobe high signal lesions (T2W, FLAIR sequences), with more severe lesions in the left lobe and no contrast enhancement, consistent with the imaging features of PML. According to the spinal tap, the patient was JC virus-positive. HIV testing indicated a significant viral load, and electroencephalogram recorded seizures.

CLINICAL DISCUSSION

JC virus reactivation causes PML, a serious brain condition in patients with weak immune systems. HIV and immunosuppressive drugs are thought to be the potential risk factors behind the reactivation of the JC virus and the appearance of PML. Symptoms like seizures and fever are not usually associated with PML, but the presence of these symptoms hints toward the complexity of the diagnosis of this case. Doctors should focus on treating the root cause of the weakened immune system to help patients. PML was identified by combining the results of an MRI scan with the patient's HIV status and the results of a spinal tap. The patient's health deteriorated even after receiving corticosteroids, acyclovir, nutritional supplements, and palliative therapy. As time passed, he developed neurological complications, respiratory failure, and ultimately death.

CONCLUSION

This case highlights the more aggressive and unique course of PML in HIV patients, it underscores the importance of assessment of the neurological symptoms in high-risk individuals. As PML carries high mortality risk it necessitates prompt diagnosis and treatment with antiretroviral drugs to slow the disease progression.