ALCOHOL AND THE NERVOUS SYSTEM

Transcription

1 iii16 ALCOHOL AND THE NERVOUS SYSTEM See end of artile for authors affiliations Correspondene to: Dr Claire MIntosh, Royal Edinburgh Hospital, Morningside Terrae, Edinburgh EH10 5HF; DETECTION A C MIntosh, J Chik J Neurol Neurosurg Psyhiatry 2004; 75(Suppl III):iii16 iii21. doi: /jnnp lohol is an available, legal, and frequently used drug in our soiety. However, its misuse and toxi effets are estimated to ost the British National Health Servie 160 million eah year in treatment osts. It is estimated that people die eah year in the UK as a result of their alohol onsumption. 1 Alohol s assoiated morbidity impats greatly on the work of the neurologist. OF ALCOHOL MISUSE Approximately 25% of male medial admissions may be regarded as problem drinkers, with the group at highest risk being young male patients admitted to medial or orthopaedi wards. 2 One of the key messages of this artile must be to always ask patients about their alohol use. This needs to be routinely doumented in notes, perhaps most usefully with a full drug use history. People may minimise their alohol use, so tat is neessary. Table 1 ontains a list of questions that may be helpful; learly it is important to get your own routine and to be guided by what the patient is able to tell you at that time. Relatives may also provide enlightening and not always orroborative histories. ALCOHOL AT A NEUROTRANSMITTER LEVEL Alohol s entral nervous system (CNS) effets are mediated through ations on a variety of neurotransmitters. There is a omplex interplay between exitatory and inhibitory systems (table 2). The numerous transmitters involved in alohol s ation explain its diverse effets and the large number of drug interations with both presribed and illiit drugs. ACUTE INTOXICATION Many pratitioners reading this artile will be aware on both a personal and oupational level of the effets of aute intoxiation. Blood alohol onentrations reflet rate of intake, degree of tolerane, and the simultaneous effets of other drugs. Extreme intoxiation (. 300 mg/100 ml) leads to inreasing drowsiness and then oma, with depressed tendon reflexes, hypotension, hypothermia, and slowed respiration. Death may our with blood alohol onentrations. 400 mg/100 ml. Severely intoxiated individuals may require admission to hospital and management in speialist units with lose monitoring and respiratory support. In those with a blood alohol onentration of, 400 mg/100 ml an alternative ause for oma must be onsidered, suh as head injury, other drug usage, hypoglyaemia or meningitis, as outlined by the Medial Counil on Alohol (see key referenes). ALCOHOL WITHDRAWAL AND NEUROTOXICITY When patients are drinking daily, or using alohol at a very high level, they may beome physially dependent on alohol (table 3). It is sometimes diffiult to predit whih patients will require detoxifiation (mediation assisted withdrawal), but levels of over 15 units/day for men and 10 units/day for women are often quoted. At a ellular level daily alohol intake indues the brain adaptations detailed in table 2, so leaving the brain with a funtional inrease in NMDA reeptor levels, part of an exitatory brain system. When alohol is stopped these exess reeptors ombine to ause a large alium flux into ells, hyperexitability, and ell death. There is also removal of alohol mediated inhibitory ations via GABA and the magnesium ontrolled inhibitory part of the NMDA reeptor. The inrease in exitatory glutamate ombined with a sudden drop in the brain s inhibitory systems ombine to give noradrenergi overdrive, leading to an inrease in sympatheti ativity. Patients who stop drinking experiene a spetrum of different symptoms ranging from mild sleep disturbane to frank delirium tremens. The severity of these relate to a number of fators, but most importantly the abruptness of withdrawal, level of alohol intake, and the ontribution of residual effets of previous drinking. J Neurol Neurosurg Psyhiatry: first published as /jnnp on 16 August Downloaded from on 30 June 2018 by guest. Proteted by opyright.

2 Table 1 The alohol history Step 1: estimate onsumption Do you ever drink alohol? What do you usually drink? How many times eah week do you drink ould you say how muh you would have on those oasions? Are there times when you would drink more heavily than this? (The MCA referene in the route map will help you quantify units and qualify them in terms of risk) Step 2: establish if they are dependent on alohol To larify, did you say that you are drinking every day? What time of day is your first drink? If you do not drink for a day, or miss your first drink of the day, how do you feel? How would you rate alohol as one of your priorities? Is it sometimes hard to think of anything else? Have you ever needed mediation to stop drinking? Step 3: eluidate any problems Has alohol ever aused you any problems in the past? Could you tell me more about that? Has anyone lose to you expressed worries about your drinking? Did this ause diffiulty between you? Are you onerned about your alohol use? Step 4: further qualify experienes and onerns You mention that you are worried about drinking harming your health ould you tell me more about that? Is it possible that the alohol you had drunk that evening may have ontributed to you beoming involved in the inident that led to your head injury? Has alohol ever affeted your work or ability to sort things out at home? Has alohol ever got you into trouble with the polie? Is your alohol use leaving you short of money? Is this diffiult to talk about for you? The linial manifestations of alohol withdrawal are detailed in table 4. In hospital inpatients it is important to onsider alohol withdrawal in individuals who beome onfused in the days following admission. Early signs may be those of autonomi overativity and tremor whih typially peak 6 24 hours after stopping drinking. Early illusory or transient halluinatory states may be a sign of more severe withdrawal, and an indiation that more mediation is required. The peak inidene for seizures is around 36 hours (usually ourring between hours) and for delirium around 72 hours. 3 The distinguishing features of delirium tremens, the most severe form of alohol withdrawal, are detailed (table 5). MANAGEMENT OF ALCOHOL WITHDRAWAL In patients with minor degrees of alohol withdrawal there is often no requirement for mediation to help with ontrol of Table 2 Alohol and neurotransmitters Dopamine: alohol inreases dopamine use in the nuleus aumbens, mediating its pleasurable effets via the ommon reward pathway of the mesolimbi system Noradrenaline: alohol release of noradrenaline (norepinephrine) ontributes to the enlivening and ativating party effets of alohol Endogenous opioids: Alohol s analgesi, pleasure, and stress reduing funtions are opioid related GABA: Alohol an potentiate GABA ( aminobutyri aid) ativity through ertain subunits of the GABA A reeptor. This aounts for alohol s anxiolyti and ataxi ations, and partially for amnesia and sedation. Glutamate: Alohol ats to blok the exitatory NMDA (N-methyl-Daspartate) reeptor, opposing glutamate ausing amnesia and other erebral depressant effets Serotonin: Alohol s stimulation of 5HT3 (5-hydroxytryptamine 3) provides the nausea assoiated with alohol use. Serotonin may also be linked to the pleasurable effets of alohol and differing brain serotonin levels may distinguish between anxious and aggressive alohol users Table 3 Alohol definitions Unit of alohol: In the UK this means a drink with 8 g of ethanol for example, half a pint of beer or a small (125 ml) glass of wine Hazardous drinking: synonymous with at risk drinking refers to drinking over 4 units per day for men and 2 units per day for women. These figures are also sometimes expressed as the weekly totals of 21 units per week for men and 14 units per week for women; the former version is more ommonly used to dissuade people from the idea that the units an be drunk in one sitting Harmful drinking is desribed in the International lassifiation of diseases as a pattern of drinking that auses damage to physial and mental health Alohol dependene: this desribes a luster of symptoms where alohol omes to dominate an individual s life with features suh as: a strong desire or ompulsion to drink diffiulty in ontrolling alohol use physiologial withdrawal when drinking redues tolerane, where inreasing doses of alohol are required neglet of other aspets of life persisting with alohol use despite evidene of harm Patients will drink on a daily basis, feel unwell if they stop drinking, and may report early morning drinking to relieve withdrawal symptoms. The medial literature is beoming inreasingly onsistent that benzodiazepines are the treatment of hoie for alohol withdrawal; however, there is less larity about whih partiular ompound is superior. 4 In linial pratie a long ating benzodiazepine is generally reommended, given in a gradually tapering dose (table 6). Courses are time limited, to maximise benefit to the patient and to minimise misuse of the drugs. Higher doses may be required in more unwell patients, and some autely unwell patients may require parenteral treatment, usually with intravenous diazepam. It is important to also remember that aute withdrawal may preipitate Wernike s enephalopathy. ALCOHOL AND SEIZURES The relation between alohol and seizures is omplex. It has been estimated that the prevalene of epilepsy in alohol dependent patients is three times that of the general population, although the prevalene of aloholism is only slightly higher in patients with epilepsy than in the general population. 5 As doumented above, abrupt essation after prolonged heavy drinking may trigger alohol withdrawal seizures, thought to be aused by abrupt deline of the brain alohol levels. Seizures may our before the blood alohol ontent Table 4 Clinial features assoiated with alohol withdrawal: symptoms usually peak between hours, subsiding by hours after the last drink Hyperativity Anxiety Tremor Mild pyrexia Tahyardia Hypertension Sweating Nausea and rething Seizures (see text) Auditory and visual halluinations, frightening, harateristially of vermin, and last usually 5 or 6 days iii17 J Neurol Neurosurg Psyhiatry: first published as /jnnp on 16 August Downloaded from on 30 June 2018 by guest. Proteted by opyright.

3 iii18 Table 5 Distinguishing features of delirium tremens, the most severe end of the alohol withdrawal spetrum Pronouned withdrawal symptoms: oarse tremor, agitation, tahyardia, and extreme autonomi over ativity, ompliated by disorientation, halluinations or delusions Ours in less than 5% of individuals withdrawing from alohol May develop from milder episodes of withdrawal, usually hours after stopping drinking Hyperpyrexia, ketoaidosis, and irulatory ollapse may develop returns to zero due to partial withdrawal either during sleep or during finanial limitations on the level of alohol provision. Withdrawal seizures an our after short bouts of drinking (1 6 days). The diagnosis of an alohol withdrawal seizure is usually made beause of the presene of other symptoms of alohol withdrawal, and a history of reent alohol misuse. There may be a geneti suseptibility to alohol withdrawal seizures. Autely, partial seizures and epilepti EEG abnormalities are not infrequent in alohol misusers. These are typial of post-traumati epilepsy, orrelating with the ommon ourrene of brain injury in alohol misusers. It has been suggested that alohol auses between 9 25% of ases of status epileptius, and this may often be the first presentation of alohol related seizures. The outome of patients with alohol related status epileptius appears more favourable, but reovery may be ompounded by an unduly prolonged post-ital state. Common auses of oult traumati brain injuries suh as parenhymal ontusions, subdural haematoma, and subarahnoid haemorrhages may oinide with or be aused by alohol misuse. Brain imaging should therefore be performed in those presenting with their first alohol related seizure. There should also be evaluation of whether a metaboli ause for seizures suh as hypoglyaemia is present or whether they may result from the use of illiit drugs, either stimulant usage or sedative drug withdrawal. Alohol is inreasingly used as part of polypharmay drug misuse, again requiring areful history taking. Alohol dependent patients also have seizures that our remotely from alohol withdrawal. The high prevalene of these seizures points to the role of alohol toxiity in seizure genesis. It has been shown that heavy alohol use leads to strutural brain hanges; that alohol use alone an lead to epilepsy annot be shown beause of the high rate of prior undiagnosed brain injury. Conern has been expressed that repeated yles of alohol exposure and withdrawal may lead to a proess termed kindling, whih ould then preipitate seizures. This hypothesis has some experimental support, but a reent large study did not show a orrelation with the number of withdrawal episodes. Previous head injury, however, was preditive of epilepsy. 5 Clinial experiene is that in repeated withdrawal episodes, symptoms tend to progress in severity, ulminating in seizures or serious psyhiatri sequelae. This may also reflet the fat that larger amounts of alohol are being systematially onsumed. THIAMINE AND MEMORY Improvements in imaging tehnology and our understanding of brain neurohemistry have started to unravel the assoiation between alohol, thiamine, and memory. It has been Table 6 Management of alohol withdrawal Optimise environment; quiet, well ventilated, adequately lit area, with reality orientation and reassurane available Moderate symptoms: tahyardia, nausea, tremor, sweats, anxiety, headahe, irritable, flu-like symptoms Oral diazepam mg up to four times daily and hourly if neessary (max 160 mg/24 hours) titrated to response. This should be dereased in a stepwise fashion over 7 days Severe symptoms: onfusion, bizarre, unooperative or aggressive behaviour Consider oral mediation; if rapid ontrol of the situation is required use intravenous diazemuls by slow injetion, up to 40 mg in divided doses during the first 30 minutes while monitored If further adjuntive treatment is required onsider haloperidol 5 10 mg intramusularly. Haloperidol an be given orally 5 mg twie daily up to 20 mg/day if further adjuntive treatment is required to maintain ontrol Large doses of benzodiazepines may lead to respiratory depression, therefore monitor pulse oximetery and respiratory rate. In omplex ases onsider oult head injury and other auses of toxi onfusion Consider Wernike- Korsakoff syndrome proposed that most organi brain syndromes in aloholi patients are variants of the Wernike-Korsakoff syndrome, and that there is no need to onsider a separate ategory of aloholi dementia. Alohol may have a diret neurotoxi effet on ortial neurons, but muh of the damage may be seondary to dienephali pathology aused by thiamine defiieny. Sanning studies have shown that Korsakoff patients (inluding those with wider ognitive impairment as well as memory impairment) have widespread erebral and subortial atrophy whih is greater than that found in the aloholi patients without amnesia. This is partiularly pronouned subortially. Magneti resonane imaging studies have also now suggested that shrinkage of the mamillary bodies is not as pathognomoni of Wernike-Korsakoff as textbooks suggest, with patients without amnesia having mamillary body damage as frequently as those with amnesia. 6 It is widely aepted that Wernike-Korsakoff syndrome is aused by thiamine defiieny. However, researh, diagnosis, and treatment in this area are hampered by a lak of aessible means to measure blood and brain thiamine, and mispereptions in diagnosis. PREVENTION AND MANAGEMENT OF WERNICKE- KORSAKOFF SYNDROME It is essential to onsider dietary and vitamin status in all patients with an alohol problem, whether they ontinue to drink or are presenting in the high risk period of alohol withdrawal. Wernike s enephalopathy is haraterised as a lassial triad of ataxia, onfusion, and ophthamolplegia. It is important to move beyond this pereption. The majority of diagnoses are made postmortem, and many patients will present not with the lassial triad, but o-morbid head injury, abnormal gait, memory disturbane, nystagmus, hypothermia, hypotension, aute onfusional state, oma, and of ourse alohol withdrawal. Korsakoff s psyhosis is desribed as an amnesti syndrome with impaired reent memory and relatively intat intelletual funtion. Patients rarely have a disrete defiit in forming new memories, often presenting with more global defiits, along a spetrum of severity. Korsakoff s is not J Neurol Neurosurg Psyhiatry: first published as /jnnp on 16 August Downloaded from on 30 June 2018 by guest. Proteted by opyright.

4 always preeded by a lear episode of Wernike s enephalopathy; more often there is an insidious ourse or a number of undiagnosed subaute episodes. It is essential to assess nutritional status in patients misusing alohol. Frequently patients will neglet their diet, deriving all of their alorifi needs from alohol, thus not ensuring an adequate oral intake of thiamine. Repeated vomiting, diarrhoea, and also the ations of alohol on the gut further serve to impair the availability of thiamine to the body. Thiamine (along with other B vitamins) ats as a oenzyme in gluose metabolism, lipid metabolism, amino aid prodution, and neurotransmitter synthesis. The body only stores approximately 30 mg of thiamine and defiieny may present within 2 3 weeks of intake easing, as daily turnover is 1 mg. The brain is partiularly sensitive to a breakdown in the omplex B vitamin dependent metabolism of gluose. Where Wernike s enephalopathy is suspeted prompt high dose parenteral treatment is required (table 7). The importane of this annot be overstated; this is a life saving treatment. In the early 1990s there was a withdrawal of the parenteral B vitamin preparation Parentrovite, following a warning from the Committee on Safety of Mediines (CSM) regarding serious adverse reations. There then followed a nine month gap before the reintrodution of parenteral preparations, during whih time there was a large shift in linial pratie. It is now felt that the inidene of anaphylati reation has been mispereived; it is reported that in the UK there were four reports to the CSM per million intravenous ampoules sold and one report per five million ampoules sold of the intramusular preparation. 7 Nevertheless, the British National Formulary (BNF) states that failities for the treatment of anaphylati reations should be available where parenteral preparations are given. There has been a move to using oral vitamin supplements, even in those autely unwell with Wernike s enephalopathy. In alohol misusers thiamine absorption is very variable, with some patients showing little or no absorption due to a redution in the sodium dependent transport mehanism aused by alohol usage and malnutrition. The presene of alohol in the gut will also derease absorption. It is unlikely that oral dosing will fulfil the daily requirement for thiamine, never mind replae the large defiits that these patients may have. Table 7 Management of Wernike-Korsakoff syndrome Detetion: Consider in all ases of alohol withdrawal, alohol misuse and dependene, head injury, and aute onfusional states. The lassial triad of symptoms is not required for diagnosis Assess nutritional status: Patients should be asked about their diet, reent vomiting/diarrhoea, and weight loss Treatment of Wernike-Korsakoff syndrome: British National Formulary reommends 2 3 pairs of high poteny intravenous Pabrinex injetions every 8 hours. This should be reassessed after 3 days, by when a notieable improvement should have ourred and treatment should ontinue as long as linial improvement ontinues. 7 Patients at risk of Wernike-Korsakoff syndrome: One pair of ampoules is reommended for 3 5 days in alohol misusers at risk of Wernike-Korsakoff syndrome that is, those with a history of malnutrition, weight loss, diarrhoea, vomiting or physial illness. 7 8 Optimal afterare: Appropriate and supportive plaement; maintenane of abstinene There is an important subgroup of patients who merit onsideration; these are patients who do not manifest linial signs of Wernike s, but who are at risk beause of poor diet, diarrhoea, vomiting, physial illness, and weight loss. There is onfliting expert opinion in this area, and a pauity of high level evidene, but the balane of probability, and the researh findings, suggest that this group of patients should also be given parenteral B vitamins. It is felt that in this group insidious or multiple subaute episodes are ourring. The debate over the role of oral vitamins ontinues. A reent evidene based guideline reommended their usage in patients who ontinued to drink and whose diet may be defiient. 8 This was on the rationale that these were inexpensive ompounds, with little assoiated harm, whih may onvey some benefit. Split dosing was reommended, to maximise absorption. There is a popular mispereption that Korsakoff s is a stati ondition, unamenable to treatment or improvement. Classially the outome from an episode of Korsakoff syndrome falls roughly into quarters, 25% showing no reovery, 25% slight, 25% signifiant, and 25% omplete reovery of memory. 9 Often patients with Korsakoff syndrome are first enountered in general medial settings where they have presented with a ompliation of their alohol misuse. One the toxi state has resolved a learer piture of defiits may be obtained. It may be the ase that patients are unable to return home beause of their memory defiits. Servies are generally poor at plaing patients who may be young and fit, but with pronouned ognitive impairment. This may lead to patients remaining on aute wards, whih an be problemati for both staff and patients. Ideally rehabilitation should be in speial units, offering to help reovery of ognitive funtion using speial tehniques. These inlude memory aids suh as diaries and personal organisers. A tehnique alled errorless learning is also used where patient s memories are refined to retain only orret solutions to problems, not the memory of failed attempts. Table 8 Pharmaologial treatments used in alohol dependene Aamprosate: Bloks GABA and redues NMDA reeptor glutamate related exitation. It may have an effet on alium influx, and it has been proposed as having a potentially neuroprotetive role in detoxifiation. It does not interat with alohol, and is presribed post detoxifiation in speialist entres as an aid to maintaining abstinene Disulfiram: Bloks aldehyde dehydrogenase, an enzyme involved in the metabolism of alohol, leading to a build up of aetaldehyde if alohol is taken. This leads to an unpleasant reation where the patient will flush, experiene headahe, palpitations, nausea, vomiting, and, with large doses, arrhythmias, hypotension, and ollapse. It is used in well motivated patients where ompliane an be supervised by a partner, olleague or by healthare staff. Beause of the nature of the disulfiram reation it should not be used in those who would be suseptible to ardiovasular disruption. Psyhosis, pregnany, and breastfeeding are also ontraindiations. Patients should arry a ard warning of the administration of alohol as it an be present in preparations suh as mouthwashes and toiletries. Naltrexone: Antagonises endogenous opioids suh as b endorphin and enephalins. By opposing mediators of the pleasurable effets of alohol it an make alohol use less rewarding and prevent exessive single session onsumption. Naltrexone is not liensed for the treatment of alohol use in Britain, but is presribed in some speialist entres and has a growing evidene base. It is mainly used in binge drinkers to attenuate the length and severity of their binges iii19 J Neurol Neurosurg Psyhiatry: first published as /jnnp on 16 August Downloaded from on 30 June 2018 by guest. Proteted by opyright.

5 iii20 It is essential that these patients are helped to abstain ompletely from alohol. They may retain the urge to drink. They have a redued tolerane to alohol and are at high risk of injury through severe intoxiation or ollapse. A further episode of Wernike-Korsakoff syndrome may be preipitated or reovery further impaired. These patients expliitly require management by a multidisiplinary team, with soial work and oupational therapy being key players. Liaison psyhiatry will be able to offer assessment and advie on management of diffiult behaviour, as well as having knowledge of loal substane misuse servie provision. NEUROPATHY AND ATAXIA Alohol misusers may develop Saturday night palsy, a foal peripheral nerve palsy as a result of nerve ompression when heavily sleeping or stuperose. Reovery is usually omplete. Chroni alohol misusers may also develop a symmetrial, bilateral mixed sensory and motor peripheral neuropathy, usually of the lower limbs. Individuals may be asymptomati or present with pain, numbness, burning feet, and hyperaesthesia. There may also be musle weakness and diminished tendon reflexes. These neuropathies are assoiated with thiamine defiieny and may show some reovery with abstinene from alohol and thiamine supplementation. An aquired erebellar syndrome with anteriosuperior vermal atrophy on imaging (omputed tomography or magneti resonane) is well reognised. Typially gait is broad based and unstable, upper limbs being rarely involved. Similarly dysarthria and disordered eye movements are infrequent and where found should prompt a searh for an alternative ause. Alohol is also assoiated with a number of other rarer neurologial presentations outwith the sope of this artile. PSYCHIATRIC SEQUELAE OF ALCOHOL MISUSE Depressive illness is ommon in alohol misusers. It is reported that as many as 80% of aloholis omplain of depressive symptoms, inluding 30% who fulfil riteria for a major depressive disorder. 10 Alohol intoxiation an be aompanied by temporary but severe depressive symptoms. It is reognised that long term alohol use an indue a depressive disorder indistinguishable from a primary depressive illness. Substane indued disorders will remit 2 4 weeks after drinking has eased without the need for antidepressants. It is therefore ommon psyhiatri pratie to try to reassess mood when patients are alohol-free, to avoid unneessary antidepressant presribing. Patients often report using alohol to try to relieve symptoms of low mood. Researh has shown some support for this onept in women, and also that depressive symptoms may be preditive of relapse. When a primary depressive illness is present, alohol may ause further lowering of mood, and its effet of removing inhibitions leaves patients vulnerable to impulsive ations inluding self harm. Anxiety disorders and alohol dependene have a reiproal ausal relation over time. Alohol is reognised for its anxiolyti and soially enlivening properties and its use as a prop in soial situations may lead to dependene. Anxiety disorders are ommonly treated using a ombination of mediation suh as serotonin reuptake inhibitors (SSRIs) and talking treatments, with an initial goal of abstinene. Alohol use predisposes to psyhoti symptoms. These an our during withdrawal, and lassially are visual halluinations. Alohol misusers may develop a halluinosis and will report halluinations whih may be a ontinuation of those experiened in aute withdrawal or may start de novo in those who are still drinking. They may start as simple sounds suh as glasses linking, but develop on to form words or sentenes. These experienes may lead to the patient forming a delusional network around them. This ondition has some similarities to shizophrenia, but differs in its age of onset, family history, and prognosis. Usually, with antipsyhoti treatment and abstinene from alohol, patients will be symptom-free at six months. Alohol misuse is ommon in shizophreni patients, and is often impliated in relapse and exaerbation of symptoms. Again it an be diffiult to eluidate the primary ondition, but abstinene from alohol improves symptoms. TREATMENT AVENUES Alohol misuse is a diffiult and sometimes frustrating ondition to treat, both for the individual involved and also sometimes for liniians. Servies vary between hospitals, with some well served by liaison and addition psyhiatry with speialist alohol nurses, and others struggling to obtain a psyhiatri assessment. Many areas will have ards or leaflets detailing loal substane misuse servies and how to ontat them. As disussed above, it is important to establish patients pereption of their drinking and to gauge their willingness to hange. If they do not regard their drinking as a problem, and are speaking to you under sufferane, a good outome an be to establish a rapport and to try to get them to reflet on their drinking. Motivational interviewing approahes, where people are gently helped to disuss their drinking behaviour and enouraged to fous on the assoiated harms, are now felt to be more helpful than statements like You are killing yourself with drink. Controlled drinking may be a viable goal for some patients, but generally in those who have reahed the levels of harmful or dependent drinking at least a period of sobriety is highly reommended. Where patients express a readiness to hange their behaviour there are a variety of approahes on offer. Postdetoxifiation there are mediations whih an be proposed (table 8). These should be used with ongoing supportive treatment. As well as mediation there are psyhologial therapies whih have been shown to help prevent relapse: behavioural self ontrol therapy, motivational enhanement therapy, marital/family therapy, and oping skills training. Loal alohol servies may run groups for patients that inorporate elements of these approahes. Lay servies have a key role in alohol treatment. Patients should have aess to information about Aloholis Anonymous and agenies suh as Counils on Alohol. Aloholis Anonymous maintains the sobriety of thousands of people. Alohol misuse has a wider effet on the family. Cliniians should be alert to onerns around domesti violene and hild protetion. Families may also have a role in helping people move into treatment servies and helping them remain there. SUMMARY Alohol is a diffiult drug to help people manage. It exerts a myriad of physial and psyhiatri effets, many of whih will J Neurol Neurosurg Psyhiatry: first published as /jnnp on 16 August Downloaded from on 30 June 2018 by guest. Proteted by opyright.

6 have impliations for the pratising neurologist. It is important to reognise when patients are experiening diffiulties with alohol and sensitively to move them towards help. In the aute inpatient situation it is important to manage withdrawal with adequate doses of benzodiazepines and onsider use of parenteral vitamins. After detoxifiation patients should be assessed for physial and psyhiatri sequelae of their alohol use and appropriate referral and treatment initiated.... Authors affiliations C MIntosh, J Chik, Royal Edinburgh Hospital, Edinburgh, UK REFERENCES (KEY*) 1 NHS Health Sotland. Alofats. A guide to sensible drinking. NHS Health Sotland, Sharpe M, Peveler R. Deliberate self harm, substane misuse and eating disorders. In: Guthrie E, Creed F, eds. Seminars in liaison psyhiatry. Gaskell, 1996: Raistrik D. Management of alohol detoxifiation. Advanes in Psyhiatri Treatment 2000;6: Mayo-Smith MF. Pharmaologial management of alohol withdrawal. A meta-analysis and evidene-based pratie guideline. Amerian Soiety of Addition working group on pharmaologial management of alohol withdrawal. JAMA 1997;278: Hillbom M, Pieninkeroinen I, Leone M. Seizures in alohol-dependent patients. Epidemiology, pathophysiology and management. CNS Drugs 2003;17: Chik J. Alohol and the brain. Current Opinion in Psyhiatry 1997;10: Cook C, Thomson A. B-omplex vitamins in the prophylaxis and treatment of Wernike-Korsakoff syndrome. Br J Hosp Med 1997;57: A brief, useful review from authors who have published widely in this area.* 8 Sottish Interollegiate Guidelines Network. The management of harmful drinking and alohol dependene in primary are, SIGN. (aessed 17 June 2004). An evidene based guideline with pratial information on sreening for alohol misuse, the management of withdrawal and use of parenteral vitamins.* 9 Smith I, Hillman A. Management of alohol Korsakoff syndrome. Advanes in Psyhiatri Treatment 1999;5: MIntosh C, Ritson B. Treating depression ompliated by substane misuse. Advanes in Psyhiatri Treatment 2001;7: Hillbom M, Pieninkeroinen I, Leone M. Seizures in alohol dependent patients: epidemiology, pathophysiology and management. CNS Drugs 2003;17: This is a thorough, up to date review of a omplex area, reommended for its larity.* 12 Nutt D. Alohol and the brain: pharmaologial insights for psyhiatrists. Br J Psyhiatry 1999;175: Explains in depth the ation of alohol at a ellular level, disussing also alohol withdrawal and treatment impliations.* 13 Medial Counil on Alohol. This website of the Medial Counil on Alohol ontains the third edition of The medial students handbook. Although this resoure has an undergraduate title it is in fat a well written and authoritative text. We reommend downloading and reading it.* iii21 J Neurol Neurosurg Psyhiatry: first published as /jnnp on 16 August Downloaded from on 30 June 2018 by guest. Proteted by opyright.