Africanised honey bee sting-induced ischaemic stroke.

The Africanised honey bee, vernacularly known as the 'killer bee', is a hybrid of the western honey bee species. These bees tend to be more aggressive with a greater tendency for swarm formation. Their stings are frequently encountered with a broad spectrum of clinical manifestations, ranging from local to systemic effects, even with recorded fatalities.

Clinical approach to the diagnosis and successful management of anti-NMDA receptor encephalitis when antibody testing is not possible.

Anti-N-methyl-D-aspartate (NMDA) receptor encephalitis is a multistage illness that progresses from psychosis, memory deficits, seizures and language disintegration to a state of unresponsiveness with catatonic features often associated with abnormal movements, and autonomic and breathing instability. While the disorder predominantly affects children and young adults, and occurs with or without tumour association, the presence of a tumour (usually an ovarian teratoma) is dependent on the age, sex and ethnicity.Teratomas present more frequently in women older than 18 years, and are more predominant in black women than Caucasians.

Amyloid pathology and axonal injury after brain trauma.

Objective: To image β-amyloid (Aβ) plaque burden in long-term survivors of traumatic brain injury (TBI), test whether traumatic axonal injury and Aβ are correlated, and compare the spatial distribution of Aβ to Alzheimer disease (AD).

Methods: Patients 11 months to 17 years after moderate-severe TBI underwent (11)C-Pittsburgh compound B ((11)C-PiB)-PET, structural and diffusion MRI, and neuropsychological examination. Healthy aged controls and patients with AD underwent PET and structural MRI.

Thalamic inflammation after brain trauma is associated with thalamo-cortical white matter damage.

Background: Traumatic brain injury can trigger chronic neuroinflammation, which may predispose to neurodegeneration. Animal models and human pathological studies demonstrate persistent inflammation in the thalamus associated with axonal injury, but this relationship has never been shown in vivo.

Findings: Using [(11)C]-PK11195 positron emission tomography, a marker of microglial activation, we previously demonstrated thalamic inflammation up to 17 years after traumatic brain injury.

Inflammation after trauma: microglial activation and traumatic brain injury.

Objective: Patient outcome after traumatic brain injury (TBI) is highly variable. The underlying pathophysiology of this is poorly understood, but inflammation is potentially an important factor. Microglia orchestrate many aspects of this response.