Neurological Problem
This paper is about the neurological problems that could arise following the use of recreational drugs and substances from a neurological perceptive. In this paper I cover general categories of recreational drugs verses specific drug by drug classifications. I present this information with minimal consideration of the added complications of the interactions between recreational drugs, alcohol, pharmacological products, and predisposing or current mental and physical health. Keep in mind that I am presenting basic neurological implications of general recreational categories. Recreational drug use is a complex, multi-layered, multi-dimensional subject matter.
It is difficult to attribute a particular clinical syndrome to a particular drug type. …show more content…
Certain common features emerge which may be related directly and specifically to the drug, but other clinical features may arise in a non-specific way from complications. Furthermore people with addictions often use more than one drug. Moreover, the dose and the constituents of what they actually take (in terms of contaminants, bases, and other substitutes) may vary according to the source, batch, etc. Lastly the effects of the drug may vary considerably according to the method of intake (orally, nasally, inhalation/smoking, intravenous, intramuscular, or subcutaneous injection), and they may be intensified by many other factors. All these factors may produce a variable clinical picture which may not be the sole cause of the neurological problems mentioned as it correlates with recreational drug use. The recognition of drug addiction raises the chance that any presenting neurological syndrome may have an unusual etiology and pathology. Management of neurological symptoms may have unpredictable difficulties and outcomes. Certain common clinical indicators are useful because their recognition may act as a ‘‘red flag’’ for drug abuse and therefore giving arise to better diagnosis, treatment, and prognosis.
Any level of the nervous system may be affected, from the cortex to the neuromuscular junction. There is a tendency to take the initial clue of drug misuse and to jump to conclusions about pathologies, and thence location of where the neurological damage is occurring. It is essential that standard diagnostic procedures are worked out first in the normal way. Then introduce history of drug use to add any “extra” pathologies that might further explain neurological symptoms over and above those of non-users.
The vast majority of patients with drug addictions seen by neurologists are seen as psychiatric hospital/crisis/detoxification emergency referrals, not as outpatient referrals.
Patients are usually young, and often remarkably young for the type of pathology presenting (for example, stroke). People with drug addictions usually present acute, with severe neurological deficits, and often have been waiting for an extraordinary time before seeking medical attention because of the additions itself, socioeconomical, and/or legal implications. The health history from the patient, relatives, or friends is often inconsistent and unreliable, or misleading. Drug misuse is usually not volunteered, but is generally admitted if directly questioned. Multiple pathologies are possible and common. It is important not to jump to rare neurological diagnosis, since a large majority of people with drug additions will be given common and mundane diagnosis and treatment with a good physical …show more content…
prognosis.
CLINICAL EFFECTS OF STIMULANTS
Examples of the stimulants include cocaine/crack, amphetamines, Ecstasy, ephedrine, and methylphenidates. These drugs share the ability to enhance transmission at the dopamine synapses and so share some common pharmacological effects and adverse effects in excess. Cross-tolerance may be seen. Those with greatest central action produce elation and increased alertness, with increased motor activity in the short and longer term (increased endurance). The motor manifestations of excess include tremors and seizures, while the neuropsychiatric manifestations include restlessness, irritability, violence, and a psychotic state (which is often paranoia). Temperature and blood pressure rise, and cardiac arrhythmias and/or sudden death may occur. In the case of cocaine, at least, there is an interaction with alcohol that increases risk of sudden death.
Acute abstinence from these stimulants is not associated with the autonomic or life threatening problems seen with alcohol and opiate dependence, but rather with disturbances of sleep, low mood and anxiety, and a craving for the drug. Stroke is the most common lasting adverse neurological event associated with the use of these stimulant drugs. Headache and/or seizures may accompany onset. The association is temporal, often very close, and this is the main evidence for a causal link, though there are also very plausible mechanisms for causation. Several potential mechanisms may apply in individual patients, and it may be impossible to disentangle the many possibilities, particularly in infarction.
Seizures may occur, particularly with the more rapid and higher levels achieved when cocaine is injected or smoked as ‘‘crack’’. In patients with pre-existing enhanced risk of seizures (for example, those with epilepsy or taking epileptic drugs), intranasal cocaine may precipitate seizures. When they do occur, seizures may be prolonged and fatal, not only through the secondary consequences of prolonged seizures but also perhaps through the direct effect of the high drug levels. Hyperpyrexia may develop because of direct effects on the hypothalamus and also the agitation and hyperactivity that these stimulant drugs tend to produce. These may contribute along with muscle vasoconstriction and central rigidity. In addition, cocaine may have a direct toxic effect on skeletal muscle (as it does on cardiac muscle).
Movement disorders have been reported with these drugs—for example, tics and acute dystonic reactions with cocaine and methamphetamine. Long term cocaine abuse has been associated with cognitive dysfunction and cerebral atrophy, and with multiple focal perfusions defected on a PET SCAN. These effects may all persist despite abstinence from the drug. Chronic amphetamine (and to a lesser extent cocaine) use may be complicated by a psychosis with visual and auditory hallucinations, often with paranoia.
CLINICAL EFFECTS OF COCAINE
About 70% of strokes arising with intranasal and intravenous use are caused by hemorrhage rather than infarction. However, the pattern of stroke may depend upon the preparation used and upon its mode of administration, since infarcts are as likely as hemorrhages when ‘‘crack’’ is smoked. This may be due to the variations of concentrations, contaminants, and whether there has been alcohol use. These factors may change the half life of how cocaine metabolizes, the metabolic pathway, and their effects on the blood vessels. The liver metabolizes cocaine with a half life of only about one hour. This may explain why most strokes occur in chronic users and/or with alcohol use. Hemorrhages may be intracerebral (basal ganglia, thalamic, lobar, or brainstem), Intraventricular or subarachnoid. They may occur especially in individuals with pre-existing vascular malformations such as aneurysms and arteriovenous malformations which accounts for up to 50% of intracranial hemorrhages with cocaine). Most strokes tend to occur within an hour of use, especially for crack and intravenous cocaine, and most of the others within three hours. The surge in blood pressure is thought to be to blame for acute rupture.
CLINICAL EFFECTS OF AMPHETAMINES
Amphetamine causes the same range of strokes as cocaine, with similar characteristics and mechanisms.
They usually occur in the first few hours after ingestion in a chronic heavy abuser, presenting with headache, an evolving focal deficit and impaired conscious level. Hemorrhages are the most common type of stroke, but even in these patients transient ischemia attack like episodes may have occurred previously. Infarction may also occur, particularly with crystal methamphetamine, which is the smoked form. Angiography may be normal but amphetamines may also be associated with beading of large arteries, or focal narrowing of arteries. Especially when used chronically and intravenously, amphetamines are the drugs most commonly associated with arrhythmias. This may be an acute hypersensitivity reaction, possibly caused by contaminants. People who abuse cocaine and amphetamines are less likely to present as clear cut strokes cases. They seem to have a more diffused neurological presentation, often with a subacute progressive time course while hospitalized, including headache, encephalopathy and/or clinical presentation of bilateral hemorrhages. Amphetamine ‘‘look-alikes’’ like ephedrine and pseudoephedrine share many of the same potential effects of amphetamines, particularly those involving the cerebral circulation. Although the risks of adverse effects occurring are less, this may be outweighed by the more widespread use and availability of these drugs in the
community.
CLINICAL EFFECTS OF SEDATIVES
Heroin is rather different from the above drugs in two major ways. Firstly it is mainly used intravenously. It can also be sniffed, smoked or injected subcutaneously. Its intravenous use often involves non-sterile needles, syringes etc, and leads to the well recognized infective complications. Not only is the entry and dissemination of organisms into the blood stream facilitated, but also people who use drugs intravenously often have a weakened immune system (for example phagocytic defects from chronic infections). Secondly the direct effects of the drug are very different. Initially there is a euphoric effect with drowsiness, though in some there will be anxiety and increased alertness. There may be nausea and vomiting. Autonomic effects (such as small pupils, difficulty passing urine, flushing, and dry mouth) may occur, but it is the suppression of respiration and coughing which are potentially the most serious, especially if vomiting occurs. With excess (and such is the variation in purity of the preparations that the dose taken is very variable), coma and deep respiratory depression are produced, along with hypotension and sometimes non-cardiogenic pulmonary edema. Cardio respiratory arrest may occur, especially if vomiting and aspiration are superimposed. Post-anoxic encephalopathy is one of the more frequent effects of heroin abuse seen by the neurologist. Coma may also result in a patient awakening with compressive nerve palsies, especially of the lateral popliteal and ulnar nerves. Characteristically they may present for attention many days later, a clue to the diagnosis in itself. The presence of bilateral synchronous sciatic nerve palsy is almost always explained by the patient passing out while sitting on the toilet, or having slid down the wall or off a seat and come to rest sitting or crouching on the floor. Compartment syndromes may also be seen after an intravenous use that has been followed by an exceptionally long coma. Although the infective complications may all be seen in patients injecting other drugs such as amphetamines or cocaine, they are much more common in heroin additions because they form the bulk of people who inject drugs.
CLINICAL EFFECTS OF BARBITUATES AND OTHER SEDATIVES
These orally taken preparations of course may also lead to coma and similar complications to those described from heroin comas, including cardiorespiratory depression (especially after barbiturates), aspiration, anoxic encephalopathy, and peripheral nerve palsies/compartment syndromes.
HALLUCINOGENS
Angel Dust was originally used as an anesthetic agent, can be used orally, nasally, or by inhalation (most commonly by smoking). It produces a mixture of effects, some stimulant, some more depressant, but abuse arose from its heightened sensory perception with eventual hallucinogenic effects. It affects many neurotransmitter systems, including those involving dopamine. It produces perceptual changes, decrease in pain sensations, and autonomic effects with flushing, sweating, raised blood pressure, and tachycardia. In higher doses, an acute delirium state develops. Convulsions or dystonic posturing may occur and the patient may progress to coma. The patients may complain of numbness, and with the combination of the anesthesia and mental changes, they may self mutilate. These adverse effects and risk of psychosis led to it falling from popularity in the 1980s. Strokes were reported in some patients.
LSD
This hallucinogenic drug alters perception, mood, and thought. However, it seems not to be associated with neurological problems. There are a few reports of cerebral infarcts with large vessel occlusion but polydrug abuse makes interpretation difficult. However, the bizarre behavior has resulted in fatal accidents and suicide. The same is also true of magic shroons.
Ketamine
Ketamine is a dissociative anesthetic, which has hallucinogenic properties and has become a drug of abuse, both ‘‘on the street’’ and in a few veterinary surgeons. The drug is still used as an anesthetic in veterinary practice and large doses can certainly produce coma in humans.
Marijuana
There is no convincing association with stroke in marijuana users. Very high doses may cause a toxic psychosis with hallucinations and paranoia. Recently the possible precipitation of more long term psychoses has been highlighted with frequent use at large doses in a still developing brain.
ORGANIC SOLVENTS
‘‘Glue sniffers’’ are usually young teenage boys and the rash and/or inflammation which often develops around the mouth and nose is an additional clue to the cause of their condition. They will experiment with all sorts of substances (lighter fluids, varnishes, paint thinners, etc) based upon organic solvents such as toluene, hexane, and benzene. Acutely these may produce a feeling of exhilaration, associated with some light headedness and giddiness, and sometimes auditory and visual hallucinations. Vomiting, tinnitus, and a later headache are additional features. The effects are short lived (for example, half an hour), often leading to repetitive use to maintain the ‘‘buzz’’. Toxicity manifests with repeated or prolonged exposure, producing impairment of coordination and cognition, with double vision, and ataxia. With increasing exposure, there is worsening disorientation, confusion, and respiratory depression that may evolve to medical coma. A confused state may last for some days, and during it only supportive treatment is possible (meaning treat the symptoms). With chronic abuse, at least of toluene, the cognitive changes and ocular motor abnormalities are unlikely to fully resolve.
CLINICAL EFFECTS OF RECREATIONAL ATHLETIC SUBSTANCES
Athletes, bodybuilders, and other gym users may use a variety of drugs for a variety of purposes:
Anabolic effects (steroids, insulin, growth hormone), stimulants to heighten alertness, reduce fatigue, and prolong endurance (amphetamines, cocaine), Erythropoietin to increase hemoglobin and oxygen delivery in endurance sports, and b2 agonists for supposed ‘‘fat-burning’’ effects.
Drugs are often obtained from underground sources or via the internet with little or no quality control and with obvious risks. Some preparations have to be injected because of significant first pass effects; with the same infection risks as for heroin addicts (needles and syringes are often shared). Neurological events are uncommon possibly because the highly trained professionals accompanying this type of lifestyle.
Works Cited
"An Official Journal of the American Academy of Neurology." Clinical Practice. Neurology Today. Web. Nov 2013. .
"Cocaine-induced cerebral vasoconstriction detected in humans with magnetic resonance angiography.." Harvard Catalyst Profiles . N.p.. Web. Nov 2013. .
Duffy, Michael. "North Shore Wales." Steroids and Illicit Drugs. SMH. Web. Nov 2013. .
"Medical aspects of drug use in the gym." . PubMed.gov. Web. Nov 2013. .
N.p.. Web. Nov 2013. .
It is difficult to attribute a particular clinical syndrome to a particular drug type. …show more content…
Certain common features emerge which may be related directly and specifically to the drug, but other clinical features may arise in a non-specific way from complications. Furthermore people with addictions often use more than one drug. Moreover, the dose and the constituents of what they actually take (in terms of contaminants, bases, and other substitutes) may vary according to the source, batch, etc. Lastly the effects of the drug may vary considerably according to the method of intake (orally, nasally, inhalation/smoking, intravenous, intramuscular, or subcutaneous injection), and they may be intensified by many other factors. All these factors may produce a variable clinical picture which may not be the sole cause of the neurological problems mentioned as it correlates with recreational drug use. The recognition of drug addiction raises the chance that any presenting neurological syndrome may have an unusual etiology and pathology. Management of neurological symptoms may have unpredictable difficulties and outcomes. Certain common clinical indicators are useful because their recognition may act as a ‘‘red flag’’ for drug abuse and therefore giving arise to better diagnosis, treatment, and prognosis.
Any level of the nervous system may be affected, from the cortex to the neuromuscular junction. There is a tendency to take the initial clue of drug misuse and to jump to conclusions about pathologies, and thence location of where the neurological damage is occurring. It is essential that standard diagnostic procedures are worked out first in the normal way. Then introduce history of drug use to add any “extra” pathologies that might further explain neurological symptoms over and above those of non-users.
The vast majority of patients with drug addictions seen by neurologists are seen as psychiatric hospital/crisis/detoxification emergency referrals, not as outpatient referrals.
Patients are usually young, and often remarkably young for the type of pathology presenting (for example, stroke). People with drug addictions usually present acute, with severe neurological deficits, and often have been waiting for an extraordinary time before seeking medical attention because of the additions itself, socioeconomical, and/or legal implications. The health history from the patient, relatives, or friends is often inconsistent and unreliable, or misleading. Drug misuse is usually not volunteered, but is generally admitted if directly questioned. Multiple pathologies are possible and common. It is important not to jump to rare neurological diagnosis, since a large majority of people with drug additions will be given common and mundane diagnosis and treatment with a good physical …show more content…
prognosis.
CLINICAL EFFECTS OF STIMULANTS
Examples of the stimulants include cocaine/crack, amphetamines, Ecstasy, ephedrine, and methylphenidates. These drugs share the ability to enhance transmission at the dopamine synapses and so share some common pharmacological effects and adverse effects in excess. Cross-tolerance may be seen. Those with greatest central action produce elation and increased alertness, with increased motor activity in the short and longer term (increased endurance). The motor manifestations of excess include tremors and seizures, while the neuropsychiatric manifestations include restlessness, irritability, violence, and a psychotic state (which is often paranoia). Temperature and blood pressure rise, and cardiac arrhythmias and/or sudden death may occur. In the case of cocaine, at least, there is an interaction with alcohol that increases risk of sudden death.
Acute abstinence from these stimulants is not associated with the autonomic or life threatening problems seen with alcohol and opiate dependence, but rather with disturbances of sleep, low mood and anxiety, and a craving for the drug. Stroke is the most common lasting adverse neurological event associated with the use of these stimulant drugs. Headache and/or seizures may accompany onset. The association is temporal, often very close, and this is the main evidence for a causal link, though there are also very plausible mechanisms for causation. Several potential mechanisms may apply in individual patients, and it may be impossible to disentangle the many possibilities, particularly in infarction.
Seizures may occur, particularly with the more rapid and higher levels achieved when cocaine is injected or smoked as ‘‘crack’’. In patients with pre-existing enhanced risk of seizures (for example, those with epilepsy or taking epileptic drugs), intranasal cocaine may precipitate seizures. When they do occur, seizures may be prolonged and fatal, not only through the secondary consequences of prolonged seizures but also perhaps through the direct effect of the high drug levels. Hyperpyrexia may develop because of direct effects on the hypothalamus and also the agitation and hyperactivity that these stimulant drugs tend to produce. These may contribute along with muscle vasoconstriction and central rigidity. In addition, cocaine may have a direct toxic effect on skeletal muscle (as it does on cardiac muscle).
Movement disorders have been reported with these drugs—for example, tics and acute dystonic reactions with cocaine and methamphetamine. Long term cocaine abuse has been associated with cognitive dysfunction and cerebral atrophy, and with multiple focal perfusions defected on a PET SCAN. These effects may all persist despite abstinence from the drug. Chronic amphetamine (and to a lesser extent cocaine) use may be complicated by a psychosis with visual and auditory hallucinations, often with paranoia.
CLINICAL EFFECTS OF COCAINE
About 70% of strokes arising with intranasal and intravenous use are caused by hemorrhage rather than infarction. However, the pattern of stroke may depend upon the preparation used and upon its mode of administration, since infarcts are as likely as hemorrhages when ‘‘crack’’ is smoked. This may be due to the variations of concentrations, contaminants, and whether there has been alcohol use. These factors may change the half life of how cocaine metabolizes, the metabolic pathway, and their effects on the blood vessels. The liver metabolizes cocaine with a half life of only about one hour. This may explain why most strokes occur in chronic users and/or with alcohol use. Hemorrhages may be intracerebral (basal ganglia, thalamic, lobar, or brainstem), Intraventricular or subarachnoid. They may occur especially in individuals with pre-existing vascular malformations such as aneurysms and arteriovenous malformations which accounts for up to 50% of intracranial hemorrhages with cocaine). Most strokes tend to occur within an hour of use, especially for crack and intravenous cocaine, and most of the others within three hours. The surge in blood pressure is thought to be to blame for acute rupture.
CLINICAL EFFECTS OF AMPHETAMINES
Amphetamine causes the same range of strokes as cocaine, with similar characteristics and mechanisms.
They usually occur in the first few hours after ingestion in a chronic heavy abuser, presenting with headache, an evolving focal deficit and impaired conscious level. Hemorrhages are the most common type of stroke, but even in these patients transient ischemia attack like episodes may have occurred previously. Infarction may also occur, particularly with crystal methamphetamine, which is the smoked form. Angiography may be normal but amphetamines may also be associated with beading of large arteries, or focal narrowing of arteries. Especially when used chronically and intravenously, amphetamines are the drugs most commonly associated with arrhythmias. This may be an acute hypersensitivity reaction, possibly caused by contaminants. People who abuse cocaine and amphetamines are less likely to present as clear cut strokes cases. They seem to have a more diffused neurological presentation, often with a subacute progressive time course while hospitalized, including headache, encephalopathy and/or clinical presentation of bilateral hemorrhages. Amphetamine ‘‘look-alikes’’ like ephedrine and pseudoephedrine share many of the same potential effects of amphetamines, particularly those involving the cerebral circulation. Although the risks of adverse effects occurring are less, this may be outweighed by the more widespread use and availability of these drugs in the
community.
CLINICAL EFFECTS OF SEDATIVES
Heroin is rather different from the above drugs in two major ways. Firstly it is mainly used intravenously. It can also be sniffed, smoked or injected subcutaneously. Its intravenous use often involves non-sterile needles, syringes etc, and leads to the well recognized infective complications. Not only is the entry and dissemination of organisms into the blood stream facilitated, but also people who use drugs intravenously often have a weakened immune system (for example phagocytic defects from chronic infections). Secondly the direct effects of the drug are very different. Initially there is a euphoric effect with drowsiness, though in some there will be anxiety and increased alertness. There may be nausea and vomiting. Autonomic effects (such as small pupils, difficulty passing urine, flushing, and dry mouth) may occur, but it is the suppression of respiration and coughing which are potentially the most serious, especially if vomiting occurs. With excess (and such is the variation in purity of the preparations that the dose taken is very variable), coma and deep respiratory depression are produced, along with hypotension and sometimes non-cardiogenic pulmonary edema. Cardio respiratory arrest may occur, especially if vomiting and aspiration are superimposed. Post-anoxic encephalopathy is one of the more frequent effects of heroin abuse seen by the neurologist. Coma may also result in a patient awakening with compressive nerve palsies, especially of the lateral popliteal and ulnar nerves. Characteristically they may present for attention many days later, a clue to the diagnosis in itself. The presence of bilateral synchronous sciatic nerve palsy is almost always explained by the patient passing out while sitting on the toilet, or having slid down the wall or off a seat and come to rest sitting or crouching on the floor. Compartment syndromes may also be seen after an intravenous use that has been followed by an exceptionally long coma. Although the infective complications may all be seen in patients injecting other drugs such as amphetamines or cocaine, they are much more common in heroin additions because they form the bulk of people who inject drugs.
CLINICAL EFFECTS OF BARBITUATES AND OTHER SEDATIVES
These orally taken preparations of course may also lead to coma and similar complications to those described from heroin comas, including cardiorespiratory depression (especially after barbiturates), aspiration, anoxic encephalopathy, and peripheral nerve palsies/compartment syndromes.
HALLUCINOGENS
Angel Dust was originally used as an anesthetic agent, can be used orally, nasally, or by inhalation (most commonly by smoking). It produces a mixture of effects, some stimulant, some more depressant, but abuse arose from its heightened sensory perception with eventual hallucinogenic effects. It affects many neurotransmitter systems, including those involving dopamine. It produces perceptual changes, decrease in pain sensations, and autonomic effects with flushing, sweating, raised blood pressure, and tachycardia. In higher doses, an acute delirium state develops. Convulsions or dystonic posturing may occur and the patient may progress to coma. The patients may complain of numbness, and with the combination of the anesthesia and mental changes, they may self mutilate. These adverse effects and risk of psychosis led to it falling from popularity in the 1980s. Strokes were reported in some patients.
LSD
This hallucinogenic drug alters perception, mood, and thought. However, it seems not to be associated with neurological problems. There are a few reports of cerebral infarcts with large vessel occlusion but polydrug abuse makes interpretation difficult. However, the bizarre behavior has resulted in fatal accidents and suicide. The same is also true of magic shroons.
Ketamine
Ketamine is a dissociative anesthetic, which has hallucinogenic properties and has become a drug of abuse, both ‘‘on the street’’ and in a few veterinary surgeons. The drug is still used as an anesthetic in veterinary practice and large doses can certainly produce coma in humans.
Marijuana
There is no convincing association with stroke in marijuana users. Very high doses may cause a toxic psychosis with hallucinations and paranoia. Recently the possible precipitation of more long term psychoses has been highlighted with frequent use at large doses in a still developing brain.
ORGANIC SOLVENTS
‘‘Glue sniffers’’ are usually young teenage boys and the rash and/or inflammation which often develops around the mouth and nose is an additional clue to the cause of their condition. They will experiment with all sorts of substances (lighter fluids, varnishes, paint thinners, etc) based upon organic solvents such as toluene, hexane, and benzene. Acutely these may produce a feeling of exhilaration, associated with some light headedness and giddiness, and sometimes auditory and visual hallucinations. Vomiting, tinnitus, and a later headache are additional features. The effects are short lived (for example, half an hour), often leading to repetitive use to maintain the ‘‘buzz’’. Toxicity manifests with repeated or prolonged exposure, producing impairment of coordination and cognition, with double vision, and ataxia. With increasing exposure, there is worsening disorientation, confusion, and respiratory depression that may evolve to medical coma. A confused state may last for some days, and during it only supportive treatment is possible (meaning treat the symptoms). With chronic abuse, at least of toluene, the cognitive changes and ocular motor abnormalities are unlikely to fully resolve.
CLINICAL EFFECTS OF RECREATIONAL ATHLETIC SUBSTANCES
Athletes, bodybuilders, and other gym users may use a variety of drugs for a variety of purposes:
Anabolic effects (steroids, insulin, growth hormone), stimulants to heighten alertness, reduce fatigue, and prolong endurance (amphetamines, cocaine), Erythropoietin to increase hemoglobin and oxygen delivery in endurance sports, and b2 agonists for supposed ‘‘fat-burning’’ effects.
Drugs are often obtained from underground sources or via the internet with little or no quality control and with obvious risks. Some preparations have to be injected because of significant first pass effects; with the same infection risks as for heroin addicts (needles and syringes are often shared). Neurological events are uncommon possibly because the highly trained professionals accompanying this type of lifestyle.
Works Cited
"An Official Journal of the American Academy of Neurology." Clinical Practice. Neurology Today. Web. Nov 2013. .
"Cocaine-induced cerebral vasoconstriction detected in humans with magnetic resonance angiography.." Harvard Catalyst Profiles . N.p.. Web. Nov 2013. .
Duffy, Michael. "North Shore Wales." Steroids and Illicit Drugs. SMH. Web. Nov 2013. .
"Medical aspects of drug use in the gym." . PubMed.gov. Web. Nov 2013. .
N.p.. Web. Nov 2013. .