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A 24-year-old immune-competent woman was admitted to hospital with a three-day history of fever and headache. On examination bilateral facial nerve palsy, lumbosacral radicular pain, reduced sacral sensibility and urinary retention were found. Open perianal lesions were suspect for genital herpes. The symptoms were compatible with a meningoradiculitis including a sacral polyradiculitis. On testing, cerebrospinal fluid was found to be abnormal with a lymphocytic cell reaction. Polymerase chain reaction (PCR) of cerebrospinal fluid and of the perianal lesions was positive for herpes simplex virus type 2 (HSV-2). An MRI scan showed colouration of part of the cauda equina. The patient was treated by intravenous injections of acyclovir 10 mg/kg t.i.d. for 21 days, after which she completely recovered. HSV-2 infection of the nervous system can cause lymphocytic, and sometimes recurrent meningitis as well as sacral polyradiculitis. It may also occur without any symptomatic genital herpes infection. A positive result from a PCR test of the cerebrospinal fluid confirms this diagnosis. Treatment with acyclovir should be started as soon as possible.

In this study, 145 healthy adults (20 to 94 years old, 69 women) were examined using ultrasound (US) imaging to obtain reference values of muscle parameters that were previously not available. We measured biceps and quadriceps sizes and subcutaneous fat thickness. To quantify muscle aspect, we defined and calculated the muscle aspect parameters muscle density, inhomogeneity and white-area index by digital image analysis. All muscle aspect parameters were found to increase with age, which may be due to age-related muscle replacement by fatty tissue and collagen. Other age-, weight- and gender-dependencies are also discussed. The complete set of muscle parameters was used to differentiate between typical myopathies and neuropathies in a group of 32 patients (24 to 79 years old, 18 women). We were successful in almost completely separating the two types of disorders based on abnormality of muscle aspect parameters alone. These preliminary results show that this set of normal muscle parameters can be used to help diagnose neuromuscular disorders. It will also facilitate follow-up in disease progression and therapy.

A 63-year-old healthy man developed acute meningitis. A Gram-stain of the cerebrospinal fluid showed Gram-negative rods, which grew slowly. They were identified by 16S ribosomal RNA sequence-analysis as Capnocytophaga canimorsus, an oral commensal found in various animal species including dogs. Upon further questioning, the patient mentioned a superficial dog bite. Using fluorescence-in situ-hybridisation with specific DNA probes, C. canimorsus cells were detected in a gingiva swab from his dog. The strains isolated from the patient and his dog were identical. The patient made a quick recovery following therapy with cefotaxime. Infections with C. canimorsus are associated with immune suppression (especially splenectomy or alcohol abuse), yet 40% of the patients have no predisposing conditions. Documented infections concern mainly sepsis or meningitis, with a mortality of approximately 30%. Due to its fastidious growth, C. canimorsus may be missed in standard culture methods. Therefore, in each case of unexplained sepsis or meningitis contact with animals should be enquired about.

Two patients, men aged 42 and 40 years, developed new neurological symptoms 3 months and 22 years, respectively, after a traumatic high thoracic spinal cord injury. The MRI scan showed a cavity in the central part of the spinal cord, on which the diagnosis of 'posttraumatic syringomyelia' could be based. In one of the patients a syringo-subarachnoidal shunt was created, the other was treated conservatively because of a severe concomitant thoracic kyphosis. Posttraumatic syringomyelia is a potentially life-threathening late complication of spinal cord injury and is characterized by development of new neurological symptoms after a variable time interval. The most typical symptom of non-traumatic syringomyelia, viz. diminution of vital sensitivity without loss of gnostic sensitivity, is not necessarily present in posttraumatic syringomyelia. Surgical treatment of posttraumatic syringomyelia is advocated if there is progressive neurological deterioration, and consists of drainage of the syrinx.

A 44-year-old man presented with painful Horner syndrome: severe periorbital pain, ptosis, and miosis of his right eye, with intact facial sweating. Lymphadenitis at the right side of his neck preceded the symptoms. MRI and magnetic resonance angiography showed thickening of the right internal carotid artery, extending from the bifurcation to the cavernous sinus, without evidence for dissection. The patient was treated with corticosteroids with immediate improvement. Control MRI scanning was normal after 6 weeks. We conclude that the painful Horner syndrome was caused by a reactive arteritis of the right internal carotid artery.

Routine determination of serum vitamin B12 levels is generally recommended as part of the screening of demented patients, based on the notion that vitamin B12 deficiency is one of the causes of reversible dementia. We studied the effects of vitamin B12 replacement therapy in a prospective longitudinal study at a memory clinic, with special emphasis on assessment of severity of dementia: not only cognitive deterioration, but also disability in the activities of daily life, behavioural problems, and the burden experienced by the caregiver were examined using instruments of proven validity. In a series of 170 consecutive patients with dementia, subnormal serum vitamin B12 levels were found in 26 cases (15%); all but one fulfilled diagnostic criteria for possible Alzheimer's disease. Cobalamin supplementation was given to all patients and the effect was evaluated after 6 months. When the size and pattern of individual change scores, and the mean change scores on all instruments were taken into account, functioning after replacement therapy was not improved. When change scores of treated patients were compared with those of patients with Alzheimer's disease (n = 69), vitamin B12 replacement did not result in slowing of the progression of dementia. Contrary to widely accepted beliefs, subnormal serum vitamin B12 levels are not a (quantitatively) important cause of reversible dementia.