COVID-19 in Sudan: Response towards control and prevention.

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Schistosomiasis of the spinal cord: report of 5 cases from Sudan.

Schistosomiasis of the spinal cord is an uncommon but potentially curable form of schistosomiasis, if diagnosed and managed early. The spinal cord is more frequently affected in Schistosoma mansoni or S. haematobium infections. This paper describes the clinical manifestations, diagnosis and management of schistosomiasis of the spinal cord in 5 patients attending Shaab and Ibn Khuldoun Hospitals, Khartoum from 1997 to 2007. There were 4 males and 1 female aged 9-45 years. They presented with symptoms and signs due to cord compression at the lower thoracic and lumbar vertebrae. Imaging studies revealed intramedullary masses compressing the cord. Biopsy showed ova of S. mansoni with surrounding inflammatory reaction. The cord showed demyelination near the ova and an associated inflammatory reaction. Patients responded well to surgical ecompression and treatment with praziquantel and oral steroids.

Schistosomiasis of the spinal cord: report of 5 cases from Sudan

Schistosomiasis of the spinal cord is an uncommon but potentially curable form of schistosomiasis, if diagnosed and managed early. The spinal cord is more frequently affected in Schistosomo mansoni or S. hoemotobium infections. This paper describes the clinical manifestations, diagnosis and management of schistosomiasis of the spinal cord in 5 patients attending Shaab and Ibn Khuldoun Hospitals, Khartoum from 1997 to 2007. There were 4 males and 1 female aged 9-45 years. They presented with symptoms and signs due to cord compression at the lower thoracic and lumbar vertebrae. Imaging studies revealed intramedullary masses compressing the cord. Biopsy showed ova of 5. mansoni with surrounding inflammatory reaction. The cord showed demyelination nearthe ova and an associated inflammatory reaction. Patients responded well to surgical decompression and treatment with praziquantel and oral steroids

Tuberculoma of the brain: a series of 16 cases treated with anti-tuberculosis drugs.

OBJECTIVES: To describe the clinical presentation, radiological findings and outcome of treatment with antituberculosis drugs in 16 cases of intracranial tuberculoma. DESIGN: Consecutive cases admitted with tuberculoma to the National Center for Neurological Diseases in Khartoum, Sudan, were included in the study. The diagnosis was based on clinical and neuro-imaging features and response to anti-tuberculosis treatment. Histopathology of material from the brain or other extracranial tissues was available in seven cases. RESULTS AND CONCLUSIONS: The commonest presenting features were headache (100%), generalized convulsions (68.7%) and hemiparesis (56.2%). Computerised axial tomography/magnetic resonance imaging (CT/MRI) showed single or multiple lesions that showed intense contrast enhancement and perilesional edema. The lesions completely cleared on anti-tuberculosis treatment in the majority of survivors (13/15). Partial clearance of lesion was associated with late presentation, multiple large lesions and advanced miliary disease. We advocate early empirical trial of anti-tuberculosis drugs for intracranial tuberculoma even after a presumptive diagnosis, particularly in areas where the infection is endemic.

Clinical presentation and CAT scan findings in mycetoma of the head.

Nine cases comprising seven males and two females with mycetoma of the cranium were studied between January 1990 and June 1997. Streptomyces somaliensis was the most common causative organism. The source of the infection was thought to be known in only three cases. The common mode of presentation was headache and scalp swelling. The next common presentation was epilepsy. Other focal neurological disorders also occur. CT scan findings of the cranium showed osteosclerotic rather than osteolytic changes.

Intraspinal mycetoma: report of two cases.

Two cases of intraspinal mycetoma caused by Madurella mycetomatis and Streptomyces somaliensis presenting with paraplegia are reported. In these cases, there was neither skin or bone involvement by the disease. The route of entry of the organisms is not known; however, hematogenous blood vessel invasion by S. somaliensis was identified in the second case.

Trigeminal afferents and brainstem centers involved in the occurrence of cerebral vasospasm.

Cisternal injections of blood in the rat and squirrel monkey produce an angiographically demonstrable biphasic vasospasm with a maximal late spasm at two days in the rat and six days post-subarachnoid hemorrhage (SAH) in the monkey. The SAH induces a decrease in cerebral blood flow of about 25% and a corresponding increase in glucose uptake of between 30% and 50%. In about half of the animals low-flow areas were noted in the cortex and the basal ganglia with a corresponding marked increase in glucose uptake. Lesioning of the A2-nucleus, its ascending pathway or the median eminence prevents the occurrence of spasm. Similarly, treatment with a substance P antagonist or gammaglobulin against substance P prevents or significantly reduces the degree of spasm. A unilateral post-ganglionic trigeminal lesion causes an ipsilateral constriction of the cerebral arteries of 27%, while a preganglionic lesion does not affect the baseline diameter. A pre- or post-ganglionic trigeminal lesion induces an increase in glucose uptake globally of about 50% without influencing cerebral blood flow. Following SAH the decrease in blood flow in both groups of lesioned animals is similar to that seen in controls. After SAH there is no further change in glucose uptake in the animals with a preganglionic lesion, while in the post-ganglionically lesioned animals there is an additional increase in glucose uptake of about 50% as compared to controls or the animals with a preganglionic lesion.

Cerebral blood flow and glucose metabolism in the squirrel monkey during the late phase of cerebral vasospasm.

A double-isotope autoradiography technique was used to evaluate cerebral blood flow (CBF) and cerebral glucose metabolism (CMRglu) during the late phase of vasospasm in a squirrel monkey subarachnoid haemorrhage (SAH) model. Cisternal blood injections induced both global and focal changes in CBF and CMRglu six days following SAH, the timepoint of maximal late spasm in this model. There was a global decrease in CBF of about 30% accompanied by an increase in deoxyglucose uptake of about 50%. Four of seven animals also had foci with flow decreased to 40% of control and deoxyglucose uptake increased to 300% of control. There was an altered but still present interdependence between flow and metabolism post SAH.

Effect of spantide, a substance-P antagonist, on cerebral vasospasm in primates.

Experimental SAH in the squirrel monkey induces an angiographically demonstrable late spasm of about 23% at six days post subarachnoid haemorrhage (SAH). The late spasm is associated with a generalized reduction in cerebral blood flow (CBF) of about 30%. Intracisternal administration of the substance P (SP) antagonist spantide two hours and three days post SAH significantly reduces the degree of late spasm and also decreases the degree of CBF reduction. The findings suggest that SP is involved in the development of both angiographical spasm and CBF changes post SAH.

Central projections of the sensory innervation to the middle cerebral artery in the squirrel monkey.

To analyze the brainstem projections of the innervation to the middle cerebral artery (MCA) in the squirrel monkey, transganglionic tracing of wheat germ agglutinin conjugated with horseradish peroxidase (WGA-HRP) was used. After application of WGA-HRP to the middle cerebral artery (MCA), labelled cell bodies were identified in the ipsilateral trigeminal and superior cervical ganglia. In the brainstem, positive labelling indicative of preterminals and terminals occurred in a discontinuous pattern throughout the trigeminal brainstem nuclear complex. At the level of the obex, nerve terminations were identified in the nucleus tractus solitarius, nucleus motorius dorsalis nervi vagi and the nucleus nervi hypoglossi. Positive WGA-HRP profiles were also observed in the periaqueductal gray matter.

Effect of pre- and postganglionic lesioning of the trigeminal nerve on cerebral blood flow and glucose metabolism following a subarachnoid haemorrhage in the squirrel monkey.

Simultaneous cerebral blood flow (CBF) and glucose metabolism (CMRglu) studies with a double isotope autoradiographic technique were applied to squirrel monkeys submitted to a unilateral pre- or postganglionic trigeminal lesion. The CBF values were not affected following a pre- or postganglionic lesion per se. In contrast, there was a global increase in the cerebral glucose uptake of about 50% as compared to controls following both kinds of lesions. Following a subarachnoid haemorrhage (SAH) 2-4 weeks after pre- or postganglionic trigeminal lesioning, there was a decrease in CBF similar to that seen in the control group. In the animals with a preganglionic lesion, the 50% increase in glucose uptake was not further augmented by a SAH and the increase in CMRglu was comparable to that found in control SAH animals. In the postganglionically lesioned monkeys, a SAH induced an additional increase in glucose uptake of about 50%. The findings suggest that the trigeminal system is involved in the regulation of cerebral metabolism via a brainstem centre.

Effect of unilateral pre- and postganglionic lesioning of the trigeminal nerve on the development of cerebral vasospasm in the squirrel monkey: angiographic findings.

Bilateral carotid angiography was performed in the squirrel monkey before and after unilateral pre- and postganglionic trigeminal lesioning. A unilateral postganglionic lesion caused a significant constriction of about 27% of the ipsilateral cerebral arteries, while a preganglionic lesion did not change the baseline arterial diameter. Following a subarachnoid haemorrhage (SAH) the degree of vasoconstriction in the animals with a preganglionic lesion did not differ significantly from that seen in controls. In the postganglionically lesioned animals, the vasoconstriction was more pronounced (12% at both 10 min and 6 days post SAH) on the lesioned as compared with the non-lesioned side. At day 6 post SAH the degree of vasoconstriction was 19% more pronounced on the lesioned side in post- as compared with the preganglionically lesioned animals. There was no difference in the degree of spasm on the non-lesioned side between the two groups. The findings indicate that the trigeminal system has both a peripheral and a central function. The peripheral, or axon reflex mechanism, exerts a tonic effect on the cerebral vessels. Following a SAH the axon reflex seems to attenuate cerebral vasospasm.

A primate model for acute and late cerebral vasospasm: angiographic findings.

A subarachnoid haemorrhage (SAH) in the squirrel monkey was produced by injection of blood via a permanently implanted catheter connected to the cisterna magna and a cannula stereotactically inserted into the interpeduncular cistern. Repeated angiographic examinations of the vertebro-basilar and right internal carotid arteries revealed a biphasic vasospasm with a maximal acute spasm at ten minutes and maximal late spasm at six days after blood injection. The present study has shown that a reproducible biphasic vasospasm can be produced in the squirrel monkey and evaluated by repeated angiographic examinations. The model is suitable in the study of basic mechanisms underlying vasospasm in a primate and, due to the size of the animal, autoradiographic evaluation of the cerebral blood flow and metabolism can be performed at an acceptable cost.

Effect of lesioning of medullary catecholamine neurons or the median eminence on the development of cerebral vasospasm in the squirrel monkey.

Injections of blood into the interpeduncular fossa and cisterna magna in the squirrel monkey produce an angiographically demonstrable, biphasic cerebral vasospasm with a maximal acute spasm at ten minutes and a maximal late spasm at six days after the subarachnoid haemorrhage (SAH). Selective lesioning of the A2 nucleus in the medulla oblongata or the median eminence in the hypothalamus prior to the SAH prevents the development of both the acute and late cerebral vasospasm. The present data indicate that the A2 nucleus and the median eminence participate in the development of vasospasm in the squirrel monkey.

Prevention of cerebral vasospasm in the rat by depletion or inhibition of substance P in conducting vessels.

Cisternal blood injection in the rat induces a biphasic angiographic vasospasm, with a maximal acute spasm at 10 minutes and a maximal late spasm at 2 days after the subarachnoid hemorrhage (SAH). Depletion of substance P-containing sensory nerves to the cerebral arteries with capsaicin prior to SAH prevents the development of both acute and late spasm. Intrathecal administration of the substance P antagonist spantide 2 hours prior to SAH also prevents the development of vasospasm, while spantide administration 1 hour before SAH only hinders the occurrence of late vasospasm. Intracisternal administration of spantide 2 hours post-SAH prevents the development of late vasospasm. This antagonist per se can induce a short-lasting dose-dependent angiographic vasoconstriction. Substance P-containing nerve fibers on the cerebral arteries could constitute the sensory link in a reflex arc system involved in the development of vasospasm in which the presence of blood in the subarachnoid space stimulates sensory substance P-containing nerve fibers on the cerebral arteries inducing a centripetal impulse to the A2-nucleus tractus solitarius setting into motion the events in the brain stem leading to acute and late vasospasm.

Enhanced vasoconstrictor effect of endothelin in cerebral arteries from rats with subarachnoid haemorrhage.

The contractile response to endothelin has been examined in cerebral arteries from rats subjected to a prior subarachnoid haemorrhage (SAH) and compared with saline-injected controls. Endothelin elicited concentration-dependent contractions of rat basilar artery segments. The endothelin-induced contractions were much stronger in the SAH compared to control animals, which suggests a role in the pathophysiology of cerebral vasospasm.

Stellate ganglion innervation of the vertebro-basilar arterial system demonstrated in the rat with anterograde and retrograde WGA-HRP tracing.

Stellate ganglia projections to cerebral arteries have been investigated with wheatgerm-agglutinated horseradish peroxidase (WGA-HRP). Injections of WGA-HRP into the stellate ganglia resulted in labelling of nerve fibres on the vertebral and basilar arteries, and their side branches. The innervation was bilateral, but with an ipsilateral predominance. After WGA-HRP application on the basilar artery, retrogradely labelled cells appeared in both stellate ganglia, but most numerously in the right ganglion (70-75%). Failure to detect stellate projections to cerebral arteries in 6-hydroxydopamine (6-OHDA)-pretreated animals indicates that these fibres are of noradrenergic sympathetic character. It is suggested that the stellate fibres follow the vertebral arteries towards the basilar artery and its branches.

The role of vasopressin in acute cerebral vasospasm. Effect on spasm of a vasopressin antagonist or vasopressin antiserum.

An experimental model of subarachnoid hemorrhage (SAH) in the Sprague-Dawley rat induces angiographically demonstrable, reproducible biphasic vasospasm of the vertebrobasilar system. The acute vasospasm is maximum at 10 minutes and the maximum late vasospasm occurs 2 days after the SAH. Brattleboro rats, which are deficient in arginine vasopressin (AVP), do not have acute vasospasm after SAH but exhibit a degree of late vasospasm that is not significantly different from that seen in Sprague-Dawley rats. Cisternal injection of AVP induced acute vasospasm in Sprague-Dawley rats with a duration similar to that seen after cisternal blood injection; however, at 2 days, the vessel diameter was normal. Intravenous AVP antagonist or intracisternal AVP antiserum administered prior to the SAH prevented the development of acute vasospasm without affecting the late phase. The data suggest that an increased release of AVP in the cerebrospinal fluid is involved in the development of acute cerebral vasospasm.

Brain stem terminations of the trigeminal and upper spinal ganglia innervation of the cerebrovascular system: WGA-HRP transganglionic study.

The central projections of the nerve fibers innervating the middle cerebral and basilar arteries were investigated by transganglionic tracing of wheat germ agglutinin conjugated with horseradish peroxidase (WGA-HRP) in the rat. WGA-HRP was applied to the exposed basilar and/or middle cerebral arteries. Sections of the brain, trigeminal and upper spinal ganglia were reacted with tetramethylbenzidine for detection of the tracer. The results demonstrate that trigeminal neurons that innervate the middle cerebral artery project to the trigeminal main sensory nucleus, pars oralis, and the dorsocaudal two-fifths of pars interpolaris of the trigeminal brain stem nuclear complex. Terminals were also visible in the ipsilateral nucleus motorius dorsalis nervi vagi (dmnX) and in the lateral nucleus tractus solitarius (nTs) bilaterally at the level of the obex. The ventral periaqueductal gray, including the dorsal raphe and C2 dorsal horn, were also innervated by nerve fibers from the middle cerebral artery. Ipsilateral trigeminal rhizotomy prior to WGA-HRP application over the middle cerebral artery impeded the visualization of nerve terminations throughout the brain stem. Pretreatment with capsaicin reduced the density of labeled neurons and terminals within the trigeminal ganglion and the brain stem, respectively, following WGA-HRP application over the middle cerebral artery. Basilar artery fibers terminate in the C2 dorsal horn, the cuneate nuclei, dmnX, and nTs bilaterally. A few projections were also labeled in the ventral periaqueductal gray. Unilateral upper two spinal dorsal rhizotomy prior to WGA-HRP application over the exposed basilar artery resulted in terminal labeling within the C2 dorsal horn, the cuneate nucleus, dmnX, and nTs contralateral to the rhizotomy, whereas the ipsilateral side was devoid of any labeling. Bilateral superior cervical ganglionectomy prior to WGA-HRP administration to the middle cerebral and basilar arteries did not alter the visualization of nerve terminations throughout the brain stem.

Effect of neonatal 6-hydroxydopamine treatment on experimental vasospasm following a subarachnoid hemorrhage in the rat.

Intracisternal injection of blood in the rat produces an angiographically demonstrable biphasic cerebral arterial vasospasm. Systemic 6-hydroxydopamine (6-OHDA) treatment in the neonatal stage, which causes a depletion of noradrenaline (NA) from both sympathetic and central NA-containing nerve fibers, prevents the development of the late spasm phase, while the acute spasm occurs to the same extent as in normal animals. The occurrence of acute spasm can be prevented by lesioning in the mesencephalon of the ascending catecholamine fibers originating in the lower brainstem and projecting to the hypothalamus. It is suggested that 6-OHDA treatment results in the altered spasm pattern via its effect on catecholamine fibers projecting between the medullary A1 and A2 nuclei and the hypothalamus. The occurrence of acute but not late spasm indicates that there is a different pathway underlying the two spasm phases.