A case report of a transient splenial lesion related to HaNDL syndrome.

BACKGROUND: Transient lesions in the splenium of the corpus callosum have been identified in many clinical cases, and often correspond to a metabolic insult to the brain. The syndrome of transient headache and neurological deficits with cerebrospinal fluid lymphocytosis (HaNDL syndrome) is a rare but under-recognised headache syndrome. CASE: A 47-year-old man presented to our hospital with a 2-week history of intermittent headache, and acute right sided hemisensory deficit. A CSF lymphocytosis was found and a diagnosis of HaNDL was made. A lesion in the splenium of the corpus callosum was identified on MRI. CSF lymphocytosis and the splenial lesion resolved on follow up 4 weeks later. CONCLUSION: These two entities are uncommon but increasingly recognised. The co-incidence in this patient raises the possibility of similar underlying pathological mechanisms, including vasomotor changes in blood vessels, cortical spreading depression and glutamate excitotoxicity leading to intra-myelinic oedema. Awareness of these entities will allow prompt diagnosis, preventing unnecessary tests and treatment, and allow appropriate patient management.

HIV-associated neurocognitive disorder.

Human immunodeficiency virus (HIV)-associated neurocognitive disorder (HAND) affects roughly half the HIV-positive population. The symptoms of cognitive slowing, poor concentration, and memory problems can impact on everyday life. Its diagnosis is validated where possible by identifying deficits in two cognitive domains on neuropsychologic testing in patients either with or without symptoms. Corroborating evidence may be found on imaging, blood tests, and cerebrospinal fluid analysis, though sensitive and specific biomarkers are currently lacking. The introduction of combined antiretroviral therapy in the 1990s has generated a therapeutic paradox whereby the number of severe cases of HAND has fallen, yet milder forms continue to rise in prevalence. New emphasis has been placed on identifying the cause of apparent ongoing HIV infection and inflammation of the central nervous system (CNS) in the face of durable systemic viral suppression, and how this equates to the neuronal dysfunction underlying HAND. The interaction with aging and comorbidities is becoming increasingly common as the HIV-positive population enters older adulthood, with neurodegenerative, metabolic, and vascular causes of cognitive impairment combining and probably accelerating in the context of chronic HIV infection. Therapies targeted to the CNS, but without neurotoxic side-effects, are being investigated to attempt to reduce the likelihood of developing, and improving, HAND.