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T Stojkovic

Publications and source records attributed to T Stojkovic.

At least 73 records · Page 4Linked to original sources
PubMed2001

[Sarcoidosis and progressive multifocal leukoencephalopathy].

A 70-year-old woman treated for sarcoidosis complained of progressive cognitive impairment and gait disability. Magnetic resonance imaging of the brain revealed a nonenhancing lesion in T1-weighted imaging in the left parieto-occipital region and sarcoidosis of the central nervous system was evoked. However, she rapidly deteriorated with posterior and cerebellar extension of the lesions, suggesting of progressive multifocal leukoencephalopathy (PML). DNA of the JC virus (JCV) was detected in the cerebrospinal fluid (CSF) by a polymerase chain reaction. Despite antiviral therapy, she died nine months after the first neurological signs. This case illustrates the possible association between sarcoidosis and PML, and underlines the interest to detect the presence of JCV in the CSF when the diagnosis of neurosarcoidosis appeared uncertain.

Aged↗
PubMed2001

[Myelopathy - Sjogren's syndrome association: analysis of clinical and radiological findings and clinical course].

Myelopathies associated with Sjögren's syndrome has been rarely described especially concerning magnetic resonance imaging (MRI) and treatment aspects. The aim of this study was to determine the clinical, laboratory and radiological features of myelopathies occurring in Sjögren's syndrome. Eleven patients were studied, 7 with an acute myelopathy and 4 with a chronic form. Acute myelopathy were clinically severe with a feature of transverse myelitis necessitating immunosuppressive drugs. On the other hand, chronic forms were closely similar to progressive multiple sclerosis (MS), for clinical and laboratory data. In 7 cases optic neuritis was found associated with myelopathy and fulfilled the diagnostic criteria of Devic's syndrome in 4 cases. The diagnosis of myelopathy associated with Sjögren's syndrome may be difficult especially compared with MS, HTLV1 or HIV myelopathy and sarcoidosis, in the chronic form but also with other vasculitis, MS or viral infection in the acute forms. However, in this last form, magnetic resonance imaging and cerebrospinal fluid data should bring to the diagnosis of Sjögren syndrome and confirmed by appropriate tests. This diagnosis will have direct consequences for an early treatment by immunosuppressive drugs.

Adult↗
PubMed2001

[Tubular aggregate congenital myopathy associated with neuromuscular block].

Various myopathies are described associated with tubular aggregates. However, in several cases tubular aggregates constitute the main structural feature allowing to consider myopathy with tubular aggregates as a distinct entity. A 50-year-old woman whose parents were consanguinous, presented frequent falls. She walked only after 18 months of age and did poorly in gymnastics. The weakness, which has myasthenic feature, involved predominantly the pelvis girdle. The serum creatine kinase was 206 UI/L (normal < 110 UI/L). Electromyogram showed a myogenic pattern in proximal muscles. Repetitive stimulation on the trapezius revealed 50 p. cent decrementing response. Muscle biopsy showed numerous tubular aggregates in type II fibers. Anti-acetylcholine receptor (AChR) antibodies were absent. There was no thymoma. The neostigmine test was negative. Clinical and electrical myasthenic features characterize one of the numerous forms of myopathy with tubular aggregates. In our case, the lack of AChR antibodies and the negative response to neostigmine argue in favor of a dysfunction of the AChR. This unusual observation highlights the therapeutic difficulties in this myopathy with neuromuscular block.

Biopsy↗
PubMed2001

[Hearing loss in multiple sclerosis: clinical, electrophysiologic and radiological study].

Clinical presentation of multiple sclerosis (MS) is highly heterogeneous. Deafness is considered to be rare. The aim of this study was to determine the frequency of acute deafness in MS and to evaluate prognosis. The occurrence of acute deafness was systematically noted in a cohort of 400 consecutive clinically definite MS patients. Acute deafness was observed in 14 patients (3.5 p. cent) with a mean age of 28 years (15 to 48) and after a mean of 2.3 years (0 to 10) of disease duration. In all but two patients, deafness was associated with disease exacerbations, highly suggestive of infratentorial lesions. MRI showed hyperintensities in the pons or the midbrain in 11 cases. Deafness disappeared in all cases excepted for one patient. After a mean follow-up of 7.2 years (1 to 17), all the patients remain in the relapsing-remitting form of the disease with a mean EDSS of 2.4 (0 to 4.5). Acute deafness is observed in 3.5 p. cent of MS cases and occurs more frequently during the first years of the disease. Although follow-up of a larger cohort is necessary, deafness could be of good prognostic factor in MS.

Adolescent↗
PubMed2000

Cardiac repolarization abnormalities in multiple sclerosis: spinal cord MRI correlates.

Ventricular repolarization dysfunction has recently been reported in multiple sclerosis (MS). We evaluated ventricular repolarization dysfunction in 52 MS patients and looked for a relationship between corrected QT (QTc) abnormalities (i.e., abnormalities of QT intervals corrected for rate) and spinal cord magnetic resonance imaging (MRI) findings. QTc intervals were increased in MS patients compared with controls (P < 0.01) and were correlated with a reduction of spinal cord area (P < 0.01). QTc abnormalities in MS were thus associated with axonal loss, reflected by spinal cord atrophy, rather than demyelination.

Adult↗
PubMed2000

Visual evoked potentials study in chronic idiopathic inflammatory demyelinating polyneuropathy.

BACKGROUND: The frequency of the association between chronic demyelinating inflammatory polyneuropathy (CIDP) and central nervous system (CNS) demyelinating lesions is probably underestimated. OBJECTIVE: To investigate the occurrence of combined central and peripheral demyelination in CIDP patients and to correlate visual evoked potential (VEP) abnormalities with CNS demyelinating lesions, observed on brain magnetic resonance imaging, and antibodies against glycolipids. METHODS: Nerve conduction studies, brain MRI and antibodies against glycolipids were prospectively studied in 17 patients who fulfilled the diagnostic criteria proposed for CIDP (Cornblath DR, Asbury AK, Albers JW, Feasby TE, Hahn AF, McLeod JG, Mendell JR, Parry GJ, Pollard JD, Thomas PK. Ad Hoc Subcommittee of the American Academy of Neurology AIDS Task Force. Research criteria for diagnosis of chronic inflammatory demyelinating polyneuropathy. Neurology, 1991;41:617-618). VEPs were performed in each case before and after 6 months treatment with either intravenous immunoglobulins (IVIG) or steroids. RESULTS: Eight patients (47%) had increased latencies in at least one eye or showed increased interocular latency difference. Four patients (23%) presented a significant high signal intensity on T2-weighted brain MRI images. Of these 4 patients, 3 had prolonged VEP latency. Two patients with delayed VEP latency had antibodies against GM1, and SGLPG and anti-sulfatides, respectively. One patient with normal VEPs also had antibodies to GM1. VEP results were not significantly modified after treatment, either with steroids or IVIG. CONCLUSION: This study confirmed the high frequency of abnormal VEPs in CIDP patients, and found that they are poorly correlated with CNS demyelinating lesions and antibodies against glycolipids. The VEP abnormalities of these patients may be explained by the susceptibility to immune-mediated damage of both the peripheral nervous system and the optic nerve.

Adolescent↗
PubMed2000

Multiple sclerosis with normal neuro-ophthalmological work-up: results of focal stimulations induced by a scanning laser ophthalmoscope.

OBJECTIVE: Visual evoked potentials (VEPs) are a very useful tool in diagnosis of multiple sclerosis (MS). Nevertheless, in some cases of the disease, VEPs are normal. The aim of this study was to evaluate the diagnostic value of focal checkerboard reversal stimulation based on opto-acoustic modulation generated by a scanning laser ophthalmoscope (SLO) in patients whose standard neuro-ophthalmological work-up was normal. METHODS: We prospectively studied 185 MS patients. In this cohort we found 30 patients with definite MS and normal neuroophthalmological work-up and we studied the diagnostic yield of focal visual stimulation in these patients. We performed focal SLO-elicited VEPs with two different spatial distributions: a central 8 x 8 degrees square field and a central 8 x 8 degrees exclusion square. The results were analysed in terms of age of the patient, course of the disease, and disability evaluated on the Expanded Disability Status Scale (EDSS). RESULTS: Mean latencies of focal VEPs were increased in MS patients compared to controls. In MS, focal stimulation allowed dysfunction of the visual system to be detected in 50% of patients who have been classified as normal according to conventional VEPs. VEP abnormalities were found to be correlated with the EDSS score (P<0.001) and the course of the disease (P<0.05). CONCLUSION: We have demonstrated the value of focal VEPs in MS diagnosis using SLO-based techniques. Further prospective work in patients with possible and probable MS should enable an evaluation of the sensitivity and specificity of this method in the early diagnosis of MS.

Adult↗
PubMed2000

Atypical form of non-Langerhans histiocytosis with disseminated brain and leptomeningeal lesions.

An 18 year old girl presented with acute visual loss. T2 weighted brain MRI showed areas of hyperintensities in the thalamic nuclei, internal capsule, lentiform nuclei, the subarachnoidal spaces, and a retrobulbar infiltration. Analysis of CSF showed numerous foamy histiocytes without malignant cells, raised protein, and depressed glucose concentration. Biopsy of the right thalamus demonstrated aggregates of histiocytes with immunohistological and ultrastructural characteristics of non-Langerhans cell histiocytosis. The patient improved with chemotherapy and corticosteroids. After 3 months of treatment, CSF analysis showed no more histiocytes. Cytological examination of CSF can be helpful for the management of patients with extensive histiocytic infiltration.

Adolescent↗
PubMed2000

Unusual MR findings of the brain stem in arterial hypertension.

MR imaging findings have been reported in only a few cases of severe arterial hypertension. We report two cases of severe paroxysmal arterial hypertension associated with unusual brain stem hyperintensity. The lesions improved dramatically after stabilization of blood pressure, suggesting that edema could be the main cause of the MR imaging-observed hyperintensity.

Adrenal Gland Neoplasms↗
PubMed2000

[Spinal cord magnetic resonance imaging in multiple sclerosis: importance of determining degree of atrophy as a marker of disease course].

Spinal cord magnetic resonance imaging (MRI) is of particular interest in the management of multiple sclerosis (MS) especially in primary progressive forms. Most of the demyelinating lesions are located in the cervical or dorsal cord. Spinal cord area reduction has been recently correlated with the progression of disability (Losseff et al., 1996, Lycklama a Nijeholt et al., 1998). The aim of this study was to confirm this first result, to assess the reproducibility of this method and to correlate demyelinating lesions with spinal cord area reduction. Fifty two patients were included and compared with 15 controls (normal subjects). T2 Sagittal and axial plane images were performed to localized hypersignal lesions. Spinal cord area was obtained by a volume acquired inversion prepared fast spoiled gradient echo acquisition (MP-Rage) sequence. We compared the mean area value with clinical parameters (age, course of the disease, expanded disability status scale ¿EDSS) and with the number and location of demyelinating lesions. Demyelinating lesions were found in 82p.100 of MS patients and in none of controls. Mean spinal cord area was closely similar to Losseff et al. (1996) results and was reduced compared with controls (p<0.001). Spinal cord reduction was correlated with disability, studied by the EDSS. Furthermore, no correlation was found between demyelinating lesions and spinal cord area reduction. This study confirms the interest of spinal cord area mesurement in MS. Spinal cord atrophy is a reliable marker for axonal loss. This method should be of particular interest for the follow-up of axonal loss in thepeutic trials especially in primary progressive MS.

Adult↗
PubMed2000

[Paraplegia episodes revealing tuberculous myelitis].

A 38 year-old woman, without previous medical history, presented, since 1993, several paraplegic fits carrying herself progressively through to a severe paraplegia. Diagnoses successively proposed were spinal cord compressions by slipped discs, spinal cord infarct and multiple sclerosis. In November 1998, the patient presented back pain and fever. Spinal cord magnetic resonance imaging (MRI) revealed a mildly enlarged dorsal cord with signal abnormalities. The lesions were isointense on T1-weighted images, hyperintense on T2-weighted images and showed a ringlike contrast enhancement. A lumbar puncture showed a trouble cerebrospinal fluid (CSF) with leucocytes 600/mm(3) (85 p.100 polynuclear), protein 6.7 g/l, glucose 0.26 g/l, chloride 109 mmol/l. The patient was first treated with parenteral unspecific antibiotherapy. Microbiological studies of blood and CSF were negative. CSF examination with polymerase chain reaction (PCR) was positive for Mycobacterium tuberculosis. Clinical (pain and fever) symptoms and CSF abnormalities decreased after antituberculous treatment. However, paraparesis remain severe. Spinal tuberculous localizations often lead to diagnostic and therapeutic errors. Improvement of spinal cord MRI sequences and using of PCR technics in CSF would contribute to reduce these difficulties.

Adult↗
PubMed2000

[Adenovirus myelitis and Epstein-Barr myelitis: two unusual viral causes with similar presentations].

We report two cases of viral myelitis, one associated with adenovirus and the other with Epstein-Barr virus. The clinical presentation and course were similar, with viral illness, paraplegia with a D4 sensory level, and fever. Spinal magnetic resonance imaging showed a T2 cervico-dorsal high intensity signal. Cerebrospinal fluid examination showed pleocytosis without oligoclonal bands. Both patients recovered after treatment with high-dose methylprednisolone. These two cases suggest a similar clinical and paraclinical pattern in viral transverse myelitis. Moreover, treatment with corticosteroids seems to be useful in viral myelitis.

Adenoviridae Infections↗
PubMed2000

[Clinical manifestations and therapeutic approach in neurosarcoidosis].

Neurological impairment is a frequent cause of morbidity and mortality in patients with sarcoidosis. The aim of this study was to evaluate the clinical manifestations of the disease, the response to corticosteroids and alternative treatments. During a 5 year period, diagnosis of neurosarcoidosis was performed in 40 patients. We retrospectively analyzed clinical, laboratory data and response to treatments. Mean age was 41.3 years (range 17-72). Mean time of follow-up was 46 months. Neurologic signs were the first symptom in 50 p. 100 of cases and an isolated manifestation in 12.5 p. 100. Central nervous system impairment was seen in 60.7 p. 100, meningitis in 27 p. 100. Other clinical manifestations were cranial nerve palsies (27 p. 100), peripheral neuropathy (33 p. 100), myopathy (16 p. 100). Eighty percent of the patients were treated by corticosteroids. Because of a lack of efficacy 40 p. 100 of patient required alternative treatment (including methotrexate, cyclophosphamide, azathioprin, cyclosporin). Complete recovery was observed in only 27.5 p. 100 of cases confirming the severity of neurosarcoidosis. Forty percent of patients were clinically stable and 10 p. 100 worsened. No patient died. This study confirms that intensive initial treatment is often necessary to prevent irreversible lesions. Alternative treatment should be rapidly initiated in resistant forms.

Adolescent↗
PubMed1999

Sensorineural deafness in X-linked Charcot-Marie-Tooth disease with connexin 32 mutation (R142Q)

OBJECTIVE: To report a family with X-linked Charcot-Marie-Tooth disease (CMTX) with proven connexin 32 (Cx32) mutation associated with deafness. METHODS: Twelve members of a CMTX family were examined clinically. Electromyography and sensory and motor conduction studies were performed in three men, two women, and a 7-year-old boy. Audiometric testing was carried out in the three men, one woman, and an 8-year-old girl. Molecular genetic analysis was performed in six men and five women. RESULTS: The three men and the 7-year-old boy had the usual sensorimotor deficit and pronounced reduction of motor nerve conduction velocity. A 15-year-old boy was asymptomatic and had only areflexia. The women had impairment of vibratory sensation and slight slowing of nerve conduction velocities. Sensorineural deafness was observed in the three men and in an 8-year-old girl without any motor or sensory deficit. Molecular genetic analysis revealed a new missense mutation located in codon 142 of the Cx32 gene leading to the substitution of an arginine by a glutamine. CONCLUSION: CMTX due to Cx32 mutations often shows interfamilial and intrafamilial phenotypic variation, which is also the hallmark of this family. The sensorineural deafness observed in this family suggests that Cx32 could play an important role in the auditory pathway.

Adult↗
PubMed1999

[Late onset of type I familial amyloid neuropathy: results of biopsy from accessory salivary glands].

Familial amyloidotic polyneuropathy (FAP) type I is usually characterized by onset in the third decade, autonomic nervous system failure, and heart block conduction occurring after the onset of neurological symptoms. A 74-year-old woman, with past medical history of a third degree heart block treated by a pace-maker, was hospitalized because of an axonal sensory-motor polyneuropathy, without autonomic dysfunction. There was no familial history. Because she complained of mouth dryness, biopsies of the labial salivary glands were performed, showing amyloid deposits. Immuno-histochemicals studies confirmed the presence of transthyretin. We analysed the transthyretin gene of the patient and her asymptomatic son, and found in both cases, the point mutation leading to the single amino acid substitution of a methionine for valine at position 30, which is typical of type I FAP. This case revealed the clinical variation of FAP type I and the interest of biopsies of the labial salivary glands in the diagnosis of polyneuropathies.

Age Factors↗
PubMed1998

Specific pattern of nitric oxide synthase expression in glial cells after hippocampal injury.

In the central nervous system (CNS), nitric oxide (NO) is thought to be involved in a variety of functions including synaptic plasticity, long term potentiation, and neurotoxicity. The aim of the present study was to investigate the expression of nitric oxide synthase (NOS) in the mouse CNS, following surgical injury to the hippocampus. NOS expression was assessed by histochemical detection of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-diaphorase) activity and immunohistochemistry of the inducible NOS (iNOS). Two days after injury to the CA1 hippocampal field, NADPH-diaphorase activity was detected in pyramidal and granular neurons and also in glial cells in the hippocampus, in contrast to the non-injured one where NADPH-diaphorase staining was observed only in a few interneurons. NADPH-diaphorase histochemistry combined with immunolabelling for GFAP and F4/80 demonstrated that these glial cells were astrocytes and microglia. This pattern of NOS expression is induced specifically after a hippocampal injury since lesion to the prefrontal or cerebellar cortex leads to NOS activity only in monocytes/macrophages like cells. Despite the large expression of NOS detected by NADPH-diaphorase histochemistry after lesioning the hippocampus, immunostaining for iNOS was confined to microglia. The fact that induction of high levels of NOS activity are detected in glial cells after a lesion to the hippocampus could be accounted for by the sensitivity of this structure to a high release of glutamate.

Animals↗