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- Ansar, Saema, et al.
(författare)
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Elevated intracranial pressure or subarachnoid blood responsible for reduction in cerebral blood flow after SAH
- 2008
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Ingår i: Cerebral Vasospasm: New Strategies in Research and Treatment. - Vienna : Springer Vienna. - 0065-1419. - 9783211757178 ; 104, s. 231-233
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Konferensbidrag (refereegranskat)abstract
- Background. The pathogenesis of cerebral ischemia after subarachnoid hemorrhage (SAH) still remains elusive. The purpose of the present study was to examine whether it is the change in intracranial pressure (ICP) or the extravasated blood that is responsible for cerebral ischemia and cerebral vasoconstriction observed following SAH. Method. Three groups of animals were studied; (1) cisternal injection of 250 mu l blood (SAH), (2) injection of 250 mu l NaCl (saline) or (3) same procedure in every detail but no fluid injection (sham). Two days after the treatment, an autoradiographic technique was used to investigate the cerebral blood flow (CBF). Findings. Both SAH (blood+ ICP) and saline injection (ICP only) resulted in significantly reduced regional and global CBF after as compared to sham/control. Conclusions. This study revealed that both the elevation of ICP and A Subarachnoid blood per se contribute approximately equally to the SAH induced effects.
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| 2. |
- Ansar, Saema, et al.
(författare)
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Subarachnoid hemorrhage induces upregulation of vascular receptors and reduction in rCBF via an ERKI/2 mechanism
- 2008
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Ingår i: Cerebral Vasospasm: New Strategies in Research and Treatment. - Vienna : Springer Vienna. - 0065-1419. - 9783211757178 ; 104, s. 65-67
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Konferensbidrag (refereegranskat)abstract
- Previous studies have shown that endothelin type B (ETB) and 5-hydroxytryptamine type IB (5-HTIB) receptors are upregulated following subarachnoid hemorrhage (SAH). The purpose of the present study was to test whether extracellular signal-regulated kinase (ERKI/2) inhibition could alter the degree of SAH induced receptor upregulation in addition to prevent the cerebral blood flow (CBF) reduction. The ERKI/2 inhibitor SB386023-b was injected intra cisternally in conjunction with and after the induced SAH in rats. Two days after SAH cerebral arteries were harvested and the contractile response to endothelin-1 (ET-I) and 5-carboxamidotryptamine (5-CT) were investigated with a myograph. The contractile responses to ET-I and 5-CT were increased after SAH compared to sham. Administration of SB-386023-b prevented the upregulated contraction elicited by application of ET-I and 5-CT in cerebral arteries. Regional CBF evaluated by an autoradiographic technique, revealed a reduced CBF by 50% after SAH this was prevented by treatment with SB-386023-b. The results indicate that an ERKI/2 mechanism is involved in cerebral vasospasm and ischemia associated with SAH.
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| 6. |
- Bjorkman, A, et al.
(författare)
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Cortical reintegration of a replanted hand and an osseointegrated thumb prosthesis
- 2007
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Ingår i: Acta Neurochirurgica. Supplementum. - 0065-1419. ; 100, s. 109-112
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Following a peripheral nerve repair the injured nerve has to re-innervate its original cortical area, a process, which is poorly understood. Errors in this cortical re-innervation have been suggested as one key reason for the generally poor clinical outcome following nerve injuries in the hand. METHOD: Functional magnetic resonance imaging (fMRI) was used to assess cortical reintegration following amputation and reattachment of bodyparts in two different situations: a patient with a hand amputation followed by immediate surgical replantation and a patient with an osseointegrated thumb prosthesis. FINDINGS: The primary motor cortex rapidly returns to a normal activation pattern after amputation followed by replantation or application of an osseointegrated prosthesis. The primary somatosenory cortex changes from an initial ipsilateral to a bilateral activation pattern. Sensory stimulation of an osseointegrated prosthesis also shows a bilateral activation pattern in the primary somatosenory cortex. CONCLUSIONS: The primary motor cortex shows a more normal activation pattern possibly because most muscles controlling the hand are proximal to the injury and can be activated after an amputation. The primary somatosensory cortex reorganises more and the activation pattern is more bilateral compared to a healthy hand. This bilateral activation pattern could represent a compensatory mechanism for the inferior tactile function in the replanted hand and the osseointegrated prosthesis.
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| 10. |
- Dahlin, Lars, et al.
(författare)
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Functional recovery and mechanisms in end-to-side nerve repair in rats
- 2007
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Ingår i: Acta Neurochirurgica. Supplementum. - Vienna : Springer Vienna. - 0065-1419. ; 100, s. 93-95
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: End-to-side nerve repair is attachment of a single distal nerve segment (recipient nerve) end-to-side to an intact donor nerve when there is a lack of proximal nerve segment after injury. The technique is currently used clinically but the mechanism(s) behind this technique are essentially unknown. METHODS: We have studied end-to-side nerve repair in the forelimb of rats, where a single distal radial nerve or an ulnar or a median, or both, nerves are attached end-to-side to an intact musculocutaneous nerve. We have studied functional recovery, origin of the regenerating axons and cell activation by the end-to-side nerve repair. FINDINGS: Functional recovery occurs after end-to-side nerve repair but is less sufficient than conventional end-to-end nerve repair or a nerve graft procedure. Sensory and motor axons grow from the musculocutaneous nerve out into the attached nerve segment(s). An injury is required to the musculocutaneous nerve to activate sensory and motor neurons as well as Schwann cells in the musculocutaneous nerve for initiation of regeneration. CONCLUSIONS: End-to-side nerve repair may be an alternative method in specific cases of complex nerve injuries to reconstruct nerve trunks when no other repair options are possible. Some functional recovery does occur but regeneration of sensory and motor axons require an injury to the neurons of the donor nerve.
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