Jeg tror tilgengæld, at det er dumt at drikke alkohol...du skriver jo, at du har været i byen. Det er godt nok langt fra nogen videnskabelig kilde, men Jønke skriver om en bekendt i en af sine erindringsbøger, der blev totalt hjernedød af at drikke igennem ovenpå en hjernerystelse.

Du lægger dig i din seng i 3 dage i træk og sover så meget så muligt. Du ser ikke fjernsyn og du forsøger så vidt så muligt at holde dit hoved fuldstændig i ro. Hvis dette lykkes, er der ikke noget at mærke efter de 3 dage.

Hvis du fortsætter med at leve dit liv som sædvanlig kan det, som the bo nævner, vare op til år før du er helt fri for symptomer, men det kan også være væk en uge efter.

Jeg har haft utallige hjernerystelser. Både alvorlige, mindre alvorlige og ganske milde, og den kur har altid hjulpet. De mest alvorlige har dog krævet op til en uge i sengen, men jeg forstår på dig, at det er en mildere hjernerystelse du har pådraget dig.

lykke til

Jeg vil ganske enkelt råde dig til at følge lægen råd.

lægen udelukkede druk nytårsaften

så du mener han godt kan tage lidt amf eller hva?

The CNS is highly vulnerable to ischemia. Neuronal death caused by ischemia is executed via a complex array of processes in which excitotoxicity plays a major role. In excitotoxicity, cell death is triggered by the overstimulation of excitatory amino acid receptors. This leads to cytotoxic levels of calcium and to subsequent activation of destructive pathways, involving among others caspases, calpains, and the generation of reactive oxygen species (Dirnagl et al., 1999; Doble, 1999).

Compounds that interfere with excitotoxicity may be used as neuroprotective therapeutic agents. Interestingly, the brain has various endogenous protection factors at its disposal (e.g., adenosine, melatonin, and estrogens) (Reiter, 1998; Hurn and Macrae, 2000; Picano and Abbracchio, 2000). Several reports have also revealed a connection between the endogenous lipid anandamide [N-arachidonoylethanolamine (AEA)] and neurodegenerative diseases (H. S. Hansen et al., 1998, 2000; Di Marzo et al., 2000b; Baker et al., 2001).

AEA mimics in part the actions of Delta 9-tetrahydrocannabinol (THC), the psychoactive compound in marijuana. Together with 2-arachidonoylglycerol (2-AG), AEA represents a class of lipids, termed endocannabinoids because of their ability to activate the CB1 and CB2 cannabinoid receptors. AEA is rapidly translocated into the cell via a transporter protein and is then immediately inactivated by a fatty acid amide hydrolase (FAAH) (Pertwee, 1997; Di Marzo et al., 1998).

Several lines of evidence indicate that AEA can serve to protect the brain against neuronal injury (H. S. Hansen et al., 1998, 2000): (1) AEA and its precursor N-arachidonoylphosphatidylethanolamine are normally found in low concentrations in the brain, but their levels increase in a calcium-dependent manner postmortem and with severe neuronal injury (Schmid et al., 1990; Kempe et al. 1996; Hansen et al., 1999; H. H. Hansen et al., 2000, 2001; Sugiura et al., 2000); (2) exogenous AEA protects cerebral neurons from in vitro ischemia (Sinor et al., 2000); (3) CB1-mediated closing of N- and P/Q-type calcium channels protects neurons against in vitro secondary excitotoxicity (Shen et al., 1996; Shen and Thayer, 1998); (4) we have demonstrated recently that THC can reduce neuronal damage via the CB1 receptor in an in vivo model of excitotoxicity (Van der Stelt et al., 2001); (5) WIN55.212, a synthetic cannabinoid, protected rat brains against focal and global ischemia (Nagayama et al., 1999); and (6) CB1 expression is enhanced in the cortical mantle zone in rats after ischemia (Jin et al., 2000). As yet, in vivo neuroprotection by AEA has never been reported.