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SUBSTANCE MISUSE FACT SHEETS CATEGORY I – CLINICAL PRESENTATIONS: withdrawal with delirium, and and 16% of patients and the onset of the syndrome may be acute, . At higher doses, ketamine can cause dream-like states gradual and evolving over several days. and hallucinations, whilst causing delirium and amnesia when Korsakoff’s syndrome: Wernicke’s can lead to taken at higher dosages. Korsakoff’s psychosis, which is characterised by amnesia, It should be noted that an acute confusional state or delirium is and irritability. very common in older people and has numerous causes Alcoholic – related (ARD): caused by long-term, including intoxication or withdrawal from substances. excessive drinking, resulting in neurological damage and 2.4 Neurological conditions associated with impaired mental processing. In general, dementia occurs in substance use people older than 65, and is a common cause of mental dysfunction. Dementia begins gradually, and progresses slowly. Coma and : Alcoholics may have cerebral Symptoms include impaired ability to plan, memory loss, predisposing them to subdural haematomas, and disordered impaired planning and apathy mimicking depression. This is coagulation rendering them liable to intracerebral caused by 's toxic effect on brain cells. Alcohol is primarily haemorrhage. Illicit drug use can increase the risk of ischaemic responsible for at least 10% of dementia cases and haemorrhagic . Drug use may be the most common (Welch, 2011). predisposing condition for stroke among patients under 35 years of age (Esse et al, 2011). The main illicit drugs associated : Chronic alcohol use can cause with stroke are , , MDMA/ecstasy, and deficiency leading to peripheral neuropathy, which phencyclidine (PCP), and lysergic acid diethylamide (LSD). is manifested in and tingling in the limbs. Lower limbs are affected more than upper, and foot and wrist drop, and distal Stroke is the most common lasting adverse neurological event and wasting may be observed (Crome & Bloor, associated with the use of drugs. There also can be 2008). damage from this condition is usually permanent, severe medical complications associated with cocaine abuse and continued drinking could lead to disability, chronic pain, and including neurological effects, including strokes, seizures, damage to arms and legs. Avoiding alcohol and improving diet headaches, cognitive dysfunction and coma, as well as can minimise the effects of the neuropathy. cardiovascular effects including disturbances of rhythm involves damage to the that and heart attacks. MDMA (ecstasy) may be associated with both Autonomic neuropathy are responsible for control of blood pressure, , intracranial haemorrhage, and cerebral infarction, sweating, bowel and bladder emptying, and digestion. It may be but the symptoms of intoxication may include , seen in chronic alcohol use, HIV/AIDS and disease. faintness, panic attacks, loss of consciousness and seizures. Methamphetamine use, too, can increase the risk of stroke. Progressive cerebellar deterioration: Alcohol misuse is the is also associated with stroke and heart attack due to most common cause of progressive cerebellar deterioration and blood clots that may form in the arteries. most likely due to deficiency. Clinically, presentation Convulsions: The most common substance related cause of may include an ataxic gait and truncal , often worse during seizures is alcohol withdrawal, occurring in 5-15% of those with periods of abstinence. Individuals with this syndrome are usually . Typically they occur 6–48 hours after last malnourished. alcohol use, typically being are generalised tonic–clonic seizures is caused by a chronic lack of niacin (vitamin B3) in the although partial seizures can also occur. Withdrawal from diet. Chronic alcohol use can also cause poor absorption which and GHB/GBL are also associated with seizures. combines with a diet already low in niacin and tryptophan to Other causes of substance related seizures include intoxication produce pellagra. Niacin (vitamin B3, nicotinic acid) and/or with cocaine, amphetamines, and 3,4- tryptophan deficiency results in skin, gastrointestinal and methylenedioxymethamphetamine (MDMA). mental abnormalities which can progress to memory Cognitive deterioration: Long-term alcohol use leads to impairment, delusions, hallucinations, dementia or delirium. cognitive deterioration ranging from mild cognitive deficits Marchiafava–Bignami Disease is a rare progressive (affecting memory, attention, concentration and decision neurological disease seen mostly in those with chronic alcohol making) to alcoholic dementia and Wernicke-Korsakoff’s problems. It is characterized by corpus callosum demyelination, psychosis. There is some evidence that long term THC necrosis and subsequent atrophy. It generally occurs in chronic (tetrahydrocannabinol) misuse leads to cognitive dysfunction. with poor nutrition. It may present acutely with Wernicke’s encephalopathy (WE): It is potentially a reversible stupor, coma or seizures, or chronically with dementia, gait neurology condition, but if untreated it is fatal in 17% of cases, problems, apraxia and ataxia. It is reliably diagnosed with MRI. with permanent brain damage occurring in 85% of those who do not receive appropriate treatment (Crome & Bloor, 2004). It is caused by lack of thiamine (vitamin B1) due to or other causes of decreased vitamin B1. The classic triad of ocular abnormalities, ataxia and confusional state are found in

2 SUBSTANCE MISUSE FACT SHEETS CATEGORY I – CLINICAL PRESENTATIONS: NEUROLOGY

Neurological deficits can be as a result of direct or indirect use of substances Direct effect Indirect effect

l Higher dose than usual (sometimes due to an unusual l Secondary effects of a coma or seizure (especially if source, or different strength) aspiration occurs)

l Speed of entry of drug (especially intravenous or l Infection risks (easy access for pathogens, impairment of when smoked) immune system, exposures to pathogens such as HIV)

l Particular sensitivity to the drug l Head trauma (accident, assault)

l Chronic/repeated use l Accompanying lifestyle changes (alcoholism, Interaction with other components of the drug or with homelessness, prostitution) adulterants that have been mixed with the drug (e.g. talcum powder, starch, sugar)

l Interaction with other drugs l Interaction with pre-existing (hypertension, arteriovenous malformation (AVM), aneurysm, right to left cardiac shunt) l Alcoholic cerebellar degeneration l Toxic delirium with amnesia (amphetamines)

(Source: Enevoldson, 2004) Common neurological conditions associated with substance use

CS TI S O ID N S IO YP T P H N /O E IS A S L V B L E O I A U T H T N M IA O A I P LC D N ST O A SE CA Headache √√√ √ Stroke √√ Seizures √√ Coma √√√√ Transient neurological deficits √ Memory impairment √√√√ Impaired concentration √√√ Wernicke-Korsakoff disease √ Alcoholic cerebellar degeneration √ Alcoholic myopathy √ Pain √ Head trauma √ 3.0 Assessment 4.0 Treatment Undertake a comprehensive substance misuse assessment of the Neurological disorder may need to be treated in the first instance. patient if possible. The full physical examination should be done However, whilst investigations and treatment are ongoing, the in order to determine to what extent the patient is intoxicated or patient may require stabilisation on the substance of in withdrawal, or both, for different substances. Patients may have dependence or detoxification from the drug of dependence in used or be dependent on more than one substance and the order that a full assessment of the disorder can be diagnosed and interactions may produce the resulting clinical picture. treated. A range of investigations may have to be undertaken in order to Medical emergencies can result from withdrawal and intoxication determine the nature of the presenting problems. from substances and need a rapid response. These include: 3 SUBSTANCE MISUSE FACT SHEETS CATEGORY I – CLINICAL PRESENTATIONS: NEUROLOGY

Delirium tremens 6.0 References and useful resources This is associated with high mortality. The mainstay of treatment Brust. J.C. (2014). Neurologic Complications. An illicit Drug Abuse. Continuim is . The aetiology is complex but improvement life long Learning in Neurology, 20.3, 642-656 will often occur with abstinence. Crome IB & Bloor, R (2008) Alcohol problems, in Murray R. et al(eds)Essential Day E, Betham, P.W., Callaghar, Kuruvilla T, and George, S (2013) Thiamire for Seizures prevention and treatment of Wernicke Karsakott syndrome in people who abuse alcohol. Cochrance Syst. Rev. doi 10. 1002/j1465 1858. CD 004033. pub3. Brain imaging should normally be performed in those with their Cochrane Database of Systematic Reviews 2013, Issue 7. Art. No.: CD004033. first alcohol related seizure, and when there are focal signs or DOI: 10.1002/14651858.CD004033.pub3.Psychiatry Cambridge University other reasons for concern. Press. pp 198-229 Wernicke’s encephalopathy Enevoldson, P (2004) Recreational drugs and their neurological consequences. Journal of Neurology, Neurosurgery & Psychiatry, ;75:iii9-iii15 If there is any risk of Wernicke’s encephalopathy, consequences doi:10.1136/jnnp.2004.045732 of not administering parenteral thiamine is catastrophic and http://jnnp.bmj.com/content/75/suppl_3/iii9.full outweighs the risks associated with its use (Welch, 2011). Day Esse, K, Fossati-Bellani, M, Traylor, A & Martin-Schild, S (2011) Epidemic of illicit drug use, mechanims of action/addiction and stroke as a health hazard. et al (2013) have done a systematic review of the use of Brain and behaviour, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3217673/ Thiamine for Wernicke’s encephalopathy. Fink P, Hansen MS, Sondergaard L, Frydenberg M (2003). Mental illness in new Alcohol-related dementia neurological patients. Journal of Neurology, Neurosurgery & Psychiatry, ( 74), 817-819. If the symptoms of alcohol dementia are identified early Goforth, H.W., Murtagh, R & Fernardez F. (2010). Neurologic Aspects of Drug enough, the effects may be reversed. The person must stop Abuse. Neurologic Clinics, 28(1) pp 199-215. drinking and start on a healthy diet, replacing the lost . McIntosh C, Chick J. Alcohol and the . Journal of Neurology, Neurosurgery & Psychiatry, 75(Suppl 3):16–21. Patients with severe are best managed Meier, M.H, Caspla, AmblerA, Marringtonte, Houts R, Keefe RS, McDonald K, with advice and support from substance misuse teams. Patients Ward A, Poulton R, Moffitt T. E. (2012) Persistent users show with harmful use of drugs and/ or alcohol or those drinking at neuropsychological decline from childhood to midlife. Proceedings of the higher risk may respond to brief advice and referred on for National Academy of Sciences. doc: specialist treatment and psychosocial intervention. http://www.pnas.org/content/109/40/E2657.abstract Serdaru M, Hausser-Hauw C, Laplane D, et al. The clinical spectrum of alcoholic Effective treatments are available and brief interventions and pellagra encephalopathy. A retrospective analysis of (1988) 22 cases studied support to change substance using behaviour through pathologically. Brain; 111:829–42 motivational enhancement therapy can have a significant The Centre for Public Health, Faculty of Health & Applied Social Science, impact on subsequent substance use. Liverpool John Moore's University, on behalf of the Department of Health and National Treatment Agency for Substance Misuse (2011) A summary of the 5.0 Referral/networks/services health harms of drugs http://www.nta.nhs.uk/uploads/healthharmsfinal-v1.pdf Where a substance misuse issue is identified, it is recommended Welch, K (2011) Neurological complications of alcohol and misuse of drugs. that contact is made with local services to discuss an Practical Neurology (11):206-219 appropriate management plan for the patient presenting to http://pn.bmj.com/content/practneurol/11/4/206.full.pdf US Department of Health and Human Sciences (2000) 10th special report to US services with a neurological problem which may be directly or Congress on . The neurotoxicity of alcohol; Chapter 2: Alcohol indirectly as a result of substance use. and the Brain: Neuroscience and Neurobehavior http://pubs.niaaa.nih.gov/publications/10report/chap02e.pdf

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