Painful hallucinations and somatic delusions in a patient with the possible diagnosis of neuroborreliosis.

Neuroborreliosis has become the most frequently recognized tick-borne infection of the nervous system in Europe and the United States. In addition to dermatological, cardiac, articular, and neurologic manifestations, psychiatric disorders such as depression, panic attacks, and schizophrenia-like psychosis can also arise. We report on a 61-year-old woman who developed a severe pain syndrome following several tick bites. She was diagnosed with neuroborreliosis; she received various courses of antibiotics over several years, but without any clinical improvement in her condition. Her eventual admission to a psychiatric ward due to mental symptoms and neuroleptic treatment led to a dramatic improvement of her pain symptoms. However, increasing delusions disclosed a psychotic episode, which ceased over time. We discuss therapeutic difficulties and psychiatric complications in the absence of a clear-cut diagnosis of neuroborreliosis. Although this patient might have suffered from late-onset schizophrenia with painful hallucinations right from the start of her disease, the case highlights psychiatric complications that might be associated with neuroborreliosis.

Processing of temporal information and the basal ganglia: new evidence from fMRI.

Temporal information processing is a fundamental brain function, which might include central timekeeping mechanisms independent of sensory modality. Psychopharmacological and patient studies suggest a crucial role of the basal ganglia in time estimation. In this study, functional magnetic resonance imaging (fMRI) was applied in 15 healthy right-handed male subjects performing an auditory time estimation task (duration discrimination of tone pairs in the range of 1,000-1,400 ms) and frequency discriminations (tone pairs differing in pitch, around 1,000 Hz) as an active control task. Task difficulty was constantly modulated by an adaptive algorithm (weighted up-down method) reacting on individual performance. Time estimation (vs rest condition) elicited a distinct pattern of cerebral activity, including the right medial and both left and right dorsolateral prefrontal cortices (DLPFC), thalamus, basal ganglia (caudate nucleus and putamen), left anterior cingulate cortex, and superior temporal auditory areas. Most activations showed lateralisation to the right hemisphere and were similar in the frequency discrimination task. Comparing time and frequency tasks, we isolated activation in the right putamen restricted to time estimation only. This result supports the notion of central processing of temporal information associated with basal ganglia activity. Temporal information processing in the brain might thus be a distributed process of interaction between modality-dependent sensory cortical function, the putamen (with a timing-specific function), and additional prefrontal cortical systems related to attention and memory. Further investigations are needed to delineate the differential contributions of the striatum and other areas to timing.

Serial positron emission tomographic findings in an atypical presentation of fatal familial insomnia.

BACKGROUND: Genetic analyses of fatal familial insomnia, a prion disease, disclose a broader range of symptoms than previously described. Although insomnia and dysautonomia have been described as hallmarks of the disease, there is substantial variability in clinical presentation. OBJECTIVE: To evaluate serial fluorodeoxyglucose positron emission tomographic and electroencephalographic findings in atypical fatal familial insomnia without clinical insomnia. PATIENT: A 63-year-old man who had a history of gait ataxia developed rapidly progressive dementia with mild dysautonomic features. Genetic investigation confirmed diagnosis of fatal familial insomnia (D178N mutation of the prion protein gene and Val/Met polymorphism on position 129 of the mutated allele) with typical neuropathologic findings. RESULTS: Clinical signs were not specific. An electroencephalogram showed scanty triphasiclike elements and general slowing. We found thalamic hypometabolism in positron emission tomographic scans to be present in a very early stage with progressive deterioration, and patchy cortical alterations showing progression over 6 months. CONCLUSIONS: In the absence of clear clinical signs, an electroencephalogram was of major diagnostic value, although its specificity in fatal familial insomnia is under debate. Selective thalamic hypometabolism seems to be an early marker in fatal familial insomnia, while cortical changes vary with clinical presentation and stage.