Acute necrotizing encephalopathy secondary to diphtheria, tetanus toxoid and whole-cell pertussis vaccination: diffusion-weighted imaging and proton MR spectroscopy findings.

We present a previously healthy 6-month-old boy who was admitted to our hospital with lethargy, hypotonia and focal clonic seizures 6 days following diptheria, tetanus toxoid and whole-cell pertussis vaccination. A diagnosis of acute necrotising encephalopathy was made with the aid of MRI, including diffusion-weighted imaging and proton MR spectroscopy.

Cyclosporine-associated leukoencephalopathy in organ transplant recipients: experience of three clinical cases.

Leukoencephalopathy is a structural alteration of cerebral white matter mainly involving damage to myelin. Several reports have linked cyclosporine (CsA) with this alteration. The clinical features vary from qualitative alterations of consciousness to neurological deficits. Magnetic resonance imaging (MRI) of the brain demonstrates the damage to the white matter, which is essential for the differential diagnosis. We describe three clinical cases of leukoencephalopathy. The first case is a 43-year-old man received a cadaveric kidney transplant using immunosuppression with of mycophenolate mofetil, prednisone, and CsA. Four months later he developed meningism and bilateral sixth nerve palsy. The second case is a 50-year-old man with a cadaveric kidney transplant received immunosuppressive treatment with azathioprine and prednisone. As a result of gouty arthritis of the ankle, azathioprine was replaced with CsA to allow addition of allopurinol. Two weeks later he developed confusion and personality changes. The third case is a 16-year-old man received a orthotopic liver transplant. Postoperatively he suffered generalized tonic-clonic seizures. In all patients the CsA levels were toxic and signs of neurological alterations were present on MRI. All patients recovered rapidly after CsA withdrawal.

Reversible spongiform leucoencephalopathy after inhalation of heated heroin.

OBJECTIVE: To describe the clinical course and imaging findings in a young man who developed a spongiform leucoencephalopathy from heroin-vapour inhalation, and to discuss the treatments which may have contributed to the unexpected favourable outcome in this case. DESIGN: Case report. SETTING: Intensive care unit of a university teaching hospital. PATIENT: A patient who developed a near fatal toxic leucoencephalopathy with impressive clinical recovery and reversible white matter changes on imaging. MEASUREMENTS AND RESULTS: Successive computed tomography scans and magnetic resonance imaging over 7 months showed evolution from bilateral extensive involvement of the cerebral white matter to almost complete resolution accompanied by the development of periventricular lesions suggestive of necrosis. Despite the fact that the patient had stretching spasms for several days, the outcome was favourable with prolonged supportive care and antioxidant therapy by ubiquinone (coenzyme Q). CONCLUSION: This case demonstrates that prolonged intensive care is of paramount importance in patients with spongiform leucoencephalopathy after inhalation of heated heroin, that abnormalities of cerebral white matter may be slowly regressive, and supports the use of coenzyme Q in severe forms of the disease.

Two episodes of leukoencephalitis associated with recombinant hepatitis B vaccination in a single patient.

Cases of central nervous system demyelination have been reported after recombinant hepatitis B vaccination, but no causal link has been clearly demonstrated. We present the first case report involving the occurrence of 2 episodes of leukoencephalitis in a previously healthy patient after vaccination and rechallenge with hepatitis B vaccine.

Interventricular methotrexate therapy for carcinomatous meningitis due to breast cancer: a case with leukoencephalopathy.

A 46-year-old woman presented with paraplegia and severe lumbago. She had had a radical mastectomy for left breast cancer 10 years earlier, and 6 months prior to presentation she completed CMF chemotherapy for treatment of retroperitoneal metastasis. CT and MRI to identify potential causes of the paraplegia and lumbago showed leptomeningeal carcinomatosis due to dissemination from invasive recurrence of the retroperitoneal tumor. An Ommaya reservoir was inserted, and infusion of intrathecal methotrexate (MTX; 5 mg twice weekly) began. Her clinical symptoms improved after receiving 53 mg MTX. However, after receiving 83 mg MTX, the patient became dizzy from leukoencephalopathy. Although administration of prednisolone mostly resolved her symptom, the patient died 9 months after the diagnosis of carcinomatous meningitis.

[Acute hemorrhagic leucoencephalitis during tuberculosis (author's transl)]. / Leucoencéphalite aigue hémorragique au cours d'une tuberculose.

The authors report a fairly typical clinico-pathological case of acute hemorragic leucoencephalitis (A.H.L.E.). Both clinical and histological features appeared particularly acute. At autopsy a visceral evolving tuberculosis was diagnosed. Such an etiological circumstance has not been, apparently, reported in cases of A.H.L.E. published as such. Three other etiological circumstances were noticed: pyuria, treatment by cephalotin and treatment by gentamycine. The physiopathogenesis of A.H.L.E. remains obscure and will not be clarified before detailed immunological studies can be performed. But the disease is rare and brisk and diagnosis usually post-mortem.

Experimental lead encephalopathy in the suckling rat: concentration of lead in cellular fractions enriched in brain capillaries.

Five-day old rats subjected to short-term (2-day) lead exposure by gastric gavage of aqueous lead acetate at the highest non-lethal dosage (1mgPb/g body weight/day) developed a hemorrhagic encephalopathy. Capillaries and microvessels isolated from brains of these rats showed abnormal morphology consisting of an increased number of irregularly dispersed endothelial nuclei and swollen, vacuolated endothelial cells. Lead was concentrated in isolated brain capillary-microvessel fractions, as demonstrated by both atomic absorption and 210Pb tracer methods. When lead exposure was continued for 20 days (at the maximal dosage regime compatible with a 60% survival rate), the rats recovered from the initial encephalopathy and capillaries and microvessels isolated from brains of these rats appeared morphologically normal. This recovery occurred despite continued high levels of lead in the blood and in the isolated capillary-microvessel fractions, suggesting that, as capillary endothelial cells mature, they are able to adapt to the presence of large amounts of lead.