Hypoxia and Medicine

mild hypoxia stimulates respiration,why does severe hypoxia depresses the same? regulation of respiration pao2 and paco2 ph effects of hypoxia on respiration

what about the effect of hypoxia on erythrocyte count? please quickly.......thanks

Need help answering this question...Describe the impact of flight & time zone changes on physiology.? I need to include the following: Causes, symptom's and effects of: Hypoxia Hyperventilation Dehydration Circadian Rhythm Effects of time zone changes on the body clock (Jet lag) I am studying Cabin Crew and trying to finish the last of my assignment and got a little stuck. Any help would be appreciated. Thanks in advance Sarah x

What are the effect and mechanisms of action of hypoxia on the respiratory movement?

If i breathed in hydrogen with the oxygen in the air would i die of hypoxia and how long will it take to die? what are the side effects leading to death

Does thumbsucking cause brain hypoxia? as well as holding the blanket upto ones nose and inhalling during 8 hours of sleep? what are the side effects?

cardiac effects of drugs? do you know what cardiac rate/changes occur due to hypoxia from respiratory depression due to heroin toxicity?

what effects will benadryl or nyquil have on me during a 3 hour flight from austin to los angeles? ok, i am a really nervous flyer and my sister and i are going to california for spring break on friday. I've never had this issue until my summer break trip last year. I hate the fact that medicine will be my only way out of extreme nervousness, and alertness for any strange increase in altitude or wierd noises! I want to try poppin' a benadryl or have a swig of nyquil but i have no idea how this will affect me 5 miles up. I know some people are going to say try reading a book, listen to music, etc..it does not work like that for me. What im really concerned about is 1. i've heard of hypoxia and i dont want to go under cardiac arrest and 2. i have to switch flights in los angeles to san jose. Any help or pointers to something else that might calm my nerves would be greatly appreciated. -ant

what is the effect of high altitude on ESR ? at high altitudes , due to hypoxia polycythemia occurs as a result of which the ESR should decrease....but some texts mention that at high altitude ESR also increases ....!!! help ?

can you give me any info on.... hypoxia (fainting), and how fetal hypoxia can affect persons in later life? hi, basically... i suffered from serious carbon monoxide poisoning along with my mother when she was pregnant with me. i was born severely underweight and my mum was given drugs in order to force her to give birth to me to survive. I was roughly 5Ibs. then as I was about 11, i discovered i needed glasses, and this has led to my sight getting worse and worse, and now im nearly 17, and its pretty shite. the opticians told me on three occasions that the arteries and veins int he back of my arms were tiny, incredibly small. i'd also started the frequent passing out stages and being always dizzy once standing up from since I was about 12, till now. it tends to go up and down. could that be a side effect of the carbon monoxide thing? my dads also got severe bowel cancer in his family... i dont know if thats relevant or not, but basically he gets this aswell.. basically, wehnever we go to the toilet, number 2 wise!!!!, if we've got bad stomachs or we're ill, we pass out while going, and its pretty god damn painful and stressing. thats another issue, i went to the doctors and they told me that it could be caused by the bowels pressure squashing nerves or vessels supplying the brain with oxygen and shizz.. thats hypoxia. i am rather underweight, and in general im average heghted but they skinny and light... any advice or stuff, or general info that can help me? cheers :) I MEANT VEINS IN THE BACK OF MY EYES! not arms xD hahaa

Medical Trivia? Eight-year-old B.J. has had asthma for 2 years since he had acute bronchitis. He is tested for allergies and demonstrated marked responses to a number of animals, pollens and molds. B.J. also has a history of asthma related to exposure to very cold weather. Please include references. Describe the pathophysiology of an acute asthma attack in B. J. following exposure to cats. Describe the early signs of an acute asthma attack and relate each of these to the changes taking place in the lungs. State and explain the effects of a prolonged asthma attack. Explain the factors contributing to severe hypoxia and acidosis in a prolonged attack. Define status asthmaticus. Explain why B. J. is likely to have frequent respiratory infections. Suggest several measures that B. J. can take to reduce anxiety and perhaps the risk of an asthma attack. Explain why a beta2-adrenergic agent is helpful in treating asthma and how it is usually administered.

Just started levalbuterol (xoponex)? Fellow users of this medication or possible doctors/nurses, how severe are the side effects of nervousness, tremors and headache? I'm experiencing all three although the worst is the headache and overall feeling of being lightheaded that are currently bugging me. I hope I didn't OD, I followed the directions. Current dosage is 1.25mg/ 6 hours (but I've kept it at 3 times a day so far) Also taking prednisone and levaquin. Diagnosis: acute bronchitis and hypoxia Forgot to mention that I am using a nebulizer -- don't want anyone thinking I am an idiot because I'm taking it as straight shots or something.

The skin and subcutaneous fat provide little insulation in hot weather but very effective insulation in...? cold weather due to what? READING 3 VASODILATION AND VASOCONSTRICTION: During times of thermal stress, heat must be dissipated into the environment or contained within the body. The body's temperature is monitored and controlled by special neurons in the hypothalamus that respond to the temperature of the surrounding blood. This has been demonstrated by experiments which found that when implanted electrodes are used to change the temperature of the hypothalamus, the body's temperature-regulating mechanisms are fully activated, even though the temperature of the rest of the body is unchanged. When the temperature of the hypothalamus is above 37 �C, the heat loss mechanisms, such as vasodilation and sweating are activated, and when the temperature is below 37 �C, the heat conserving and heat generating mechanisms, such as vasoconstriction and shivering, are activated [12]. The body uses changes in blood circulation and changes in the thickness of the skin to control heat loss under different temperature conditions. The rate of heat conductance to the surrounding environment is influenced by the "countercurrent" system of blood flow [13]. This employs two systems of venous blood flow in the limbs: the deep venea and peripheral veins. In addition, subcutaneous fat enhances the control of insulation achieved by changes of peripheral blood flow [14,15]. In a cold environment most of the venous return from arms and legs is through the deep venea comitantes that receive heat from blood flowing through the arteries and thereby minimizes heat loss. Thus heat conductance to the periphery is low, yet actual blood flow to the limbs may be high, protecting tissues of the limbs from cold injury and hypoxia. In a hot environment most of the venous blood flow returns through the peripheral veins, and because they are close to the surface, heat loss to the environment is increased. By this pathway, external heat loss is maximized with high conductance [13]. When the blood vessels of the skin are dilated, the subcutaneous fat can have little effect, since warm blood is moving through to the surface, where heat exchange with the surrounding can take place [14]. The dermis-epidermis combination changes effective thickness by virtue of involuntary, lateral muscle movements which govern the depth of blood capillaries carrying the heat energy to be thrown away: in the cold these capillaries retract, thus increasing the effective thickness of the insulation [15]. After vasoconstriction of the blood vessels at the dermis-epidermis, this shunt no longer exists, and heat exchange must take place through the fat [14]. A. Capillary retraction B. Lateral muscle movements C. Vasoconstriction D. All of the above causes the skin and subcutaneous fat to insulate effectively in cold weather.

What happens to a pregnant woman in a hypobaric chamber? It is very possible that i am pregnant and In my job i frequently enter into hypobaric chambers (as an instructor)....even though I am always hooked up to oxygen, i know the the effects of the low atmospheric pressure on the body (gases expanding, decompression (which i have had), barotrauma, hypoxia, etc.) but i am not quite sure what would happen to a fetus or my womb if i was indeed pregnant. So my question is, is it safe for me to go inside if i MIGHT be pregnant or should i tell my boss that i cant until i know for sure (which would be bad.....) Two of our instructors are out of the country and I HAVE to go in this week.....if we cancel it will be very bad... any advice would be appreciated oh and if i am preg then i am only about 5 weeks along oh and for those that don't know what a hypobaric chamber is, it is an uncompressed high altitude simulator for low atmospheric pressure. and i go up to 25,000 w/o any pressurization and sometimes do rapid decompression (go up to 8,000 ft and then in one second go up to about 23,000 ft)....i can be at high altitudes for up to and hour

how does hypoxia effect the kidneys?

Does anyone know how hypoxia at birth could effect a child? MY son wasnt breathing when he was born ,the hospital gave me dia morphine when i was in labour and it stopped his heart. he has slurred speach and although he can walk it just doesnt look right like, he goes up on his toes alot and doesnt have good balance . The doctors say he has a global developmental delay. does anyone have any information that might help me?

does anyone have information on nootropil smart drug? ive heard about these new drugs and was wondering if anyone has had any experiences,do they work? my son had hypoxia at birth would they help him? would they help my friend with ms? has anyone taken them what effects did they have.

nootropil smart drug? ive heard about these new drugs and was wondering if anyone has had any experiences,do they work? my son had hypoxia at birth would they help him? would they help my friend with ms? has anyone taken them what effects did they have.

bradyasystolic rhythms? how do you think severe hypoxia may cause bradyasystolic rhythms? is it a direct effect on the heart itself or an indirect effect on the heart?

hematology testing? it was suggested to my son that he have neurtoxicology, hypoxia/anoxia & neuroimmunology screenings done, also to look for toxins/heavy metals, lead etc...what tests exactly do we request?? it seems that we can't get an answer nor much help from our pmd nor from the neuro dr. that he is seeing. he has been to brain matters in Colorado & had a pet scan done 1 yr ago & they suggested that we follow up at home, but again, we seem to be hitting a brick wall, all they want to do is to keep trying him on meds for bipolar which do not help him at all, the side effects are not worth keeping him on the meds.. He strongly feels that ther may be something else going on and possibly the testing may help us or let us know that there is nothing else. If possible, i would like to know exactly how these test are performed, the more info we have the better educated we are as to what to expect. i would greatly appreciate any help whatso ever.. we are just trying to get him well..thanks sooo much..

bradyasystolic rhythms? how do you think severe hypoxia may cause bradyasystolic rhythms? is it a direct effect on the heart itself or an indirect effect on the heart?

A 90% Cancer Cure Diet using Flaxseed Oil & Cottage Cheese?

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Please read this? Neurologic complications of cocaine, amphetamine, and their derivatives By: Douglas J Lanska MD MS MSPH FAAN Veterans Affairs Medical Center Great Lakes VA Healthcare System, Tomah, WI Department of Neurology University of Wisconsin, Madison, WI Abuse of certain illicit drugs can be complicated by ischemic stroke, intracerebral or subarachnoid hemorrhage, and other neurologic complications (Mathew and Wilson 1991; Baquero and Alfaro 1994; Auer et al 2002). Such agents include the sympathomimetic drugs cocaine and amphetamine, and their derivatives, including "crack," methamphetamine ("meth" or "crystal" or "speed"), "ecstasy," and "eve." Cocaine and amphetamine are strong risk factors for stroke in adolescents and young adults in most (Kaku and Lowenstein 1990; Petitti et al 1998), but not all (Qureshi et al 1997; 2001) epidemiological studies. There are multiple pathophysiological mechanisms for the cerebrovascular diseases related to use of these drugs, including vasospasm, altered platelet function, excitotoxicity, hyperthermia, and acute severe hypertension, which can cause endothelial disruption, loss of cerebral autoregulation, and hemorrhage. In many cases with abuse of such drugs, intracerebral hemorrhage is associated with an underlying vascular malformation (Klonoff et al 1989; Levine et al 1991; Daras et al 1994; Konzen et al 1995; Fessler et al 1997; McEvoy et al 2000; Auer et al 2002). In addition, individuals who abuse such drugs are also potentially susceptible to particulate embolization (from contaminants injected with intravenous drug abuse), cardiac arrhythmias, mycotic aneurysms, and endocarditis. Synergistic vasoconstrictive effects may occur with combined use of sympathomimetic agents in both human reports (Lambrecht et al 1993; Vallee et al 1993) and animal models (Wang et al 1990). Interestingly, basilar artery vasospasm has been produced in animal models by combined administration of cocaine and amphetamine (Wang et al 1990) and basilar artery thrombosis has been reported with combined abuse of cocaine and "ecstasy," an amphetamine derivative (Vallee et al 1993). Cocaine. Cocaine (benzoylmethylecgonine) is a potent sympathomimetic and CNS stimulant derived from the leaves of the shrub Erythroxylon coca, which grows primarily on the slopes of the Andes mountains in South America (Klein et al 2000; Lange and Hillis 2001). Cocaine is administered by inhalation (of smoked "crack," ie, the freebase or alkaloidal form which can be smoked), intranasally ("snorting"), and intravenously ("mainlining"), or less commonly orally ("chewing"; it is poorly absorbed by the gastrointestinal tract), intramuscularly, intravaginally, sublingually, or rectally. Cocaine hydrochloride is a water-soluble powder or granule that is readily absorbed through all mucous membranes, but that decomposes when heated, whereas alkaloidal or freebase cocaine is heat-stable and can be smoked. Alkaloidal or freebase cocaine is known as "crack" because of the popping sound that it produces when heated. Crack cocaine is the most potent and most addictive form of the drug, and smoking it can deliver cocaine to the circulation within seconds to minutes producing a short-lasting euphoria or "high." Although cocaine itself is metabolized by plasma and liver cholinesterases and is detectable in blood or urine only for several hours after use, cocaine metabolites can be detected in blood or urine for 24 to 36 hours after use, and in hair for weeks or months. Cocaine is frequently abused by adolescents and young adults in the United States (Brown et al 1992; Moliterno et al 1994; Hollander 1995; Lange and Hilllis 2001). Particularly since 1983, with the introduction of "crack" (alkaloidal or freebase form of cocaine), use of cocaine in the United States has increased dramatically (Daras et al 1994). Twenty three to 30 million Americans have used cocaine at least once (including reportedly over 30% of men and 20% of women between ages 26 and 34 years), and 2 to 5 million use it regularly (Moliterno et al 1994; Hollander 1995; Lange and Hillis 2001). Cocaine is responsible for approximately 30% of all drug-related visits to emergency rooms (Hollander 1995; Lange and Hillis 2001). When given systemically, cocaine's effects are mediated through modulation of synaptic transmission (Lange and Hillis 2001). Cocaine causes powerful sympathomimetic effects by blocking presynaptic reuptake of norepinephrine, epinephrine, and dopamine, while also stimulating the presynaptic release of norepinephrine, causing excess amounts of these neurotransmitters to stimulate the corresponding postsynaptic receptors, particularly alpha receptors peripherally (Hollander 1995; Lange and Hillis 2001). The pathogenesis of cocaine-related neurologic complications is heterogeneous, and depends in part on the dose administered and the form of cocaine used (Levine et al 1991). Abuse of alkaloidal ("crack") cocaine results in approximately equal frequencies of ischemic and hemorrhagic strokes, while cocaine hydrochloride is much more likely to be associated with hemorrhagic stroke (approximately 80% of the time) (Levine et al 1991). Cardiovascular, neurologic, and psychiatric complications are common with cocaine abuse (Moliterno et al 1994; Hollander 1995; Lange et al 2001; Kloner and Rezkalla 2003). Acute toxicity is dose-related and characterized by sympathomimetic effects, including acute and possibly profound hypertension, headache, tachycardia, hyperthermia, cardiac arrhythmias, and possibly seizures (Klein et al 2000). In some cases, profound acute toxicity occurs from rupture of packets of cocaine that have been ingested or inserted into the vagina or rectum by drug smugglers ("body packers" or "mules") (Levine et al 1990; Klein et al 2000). Cocaine, especially recent use of cocaine, is the illicit drug used most frequently in drug-related strokes (Kaku and Lowenstein 1990); the relative risk for stroke among drug abusers is 6.5 compared with nondrug abusers, and this increased to 49.4 for patients whose symptoms began within 6 hours of drug administration (Kaku and Lowenstein 1990). The higher potency of crack compared with cocaine hydrochloride has been associated with a marked increase in the frequency of cocaine-related strokes (Klonoff et al 1989; Daras et al 1994). Stroke may follow the use of cocaine by any route of administration (Klonoff et al 1989). Cocaine can produce severe cerebral vasospasm, multifocal or diffuse cerebral ischemia, ischemic and hemorrhagic stroke, intracerebral hemorrhage (particularly in the basal ganglia, but also in the deep cerebral hemispheres and the brainstem), subarachnoid hemorrhage, seizures, movement disorders, dizziness, anxiety, paranoia, hallucinations, insomnia, confusional states, stupor and coma, and possibly vasculitis (Klonoff et al 1989; Meza et al 1989; Nalls et al 1989; Sloan et al 1991; Brown et al 1992; Sloan and Mattioni 1992; Daras et al 1994; Reeves et al 1995; Nolte et al 1996; Johnson 1998a; Klein et al 2000; Broderick et al 2003; Buttner et al 2003; Vallee et al 2003; Bolouri and Small 2004). Cocaine is a major risk factor for aneurismal subarachnoid hemorrhage in young people (Levine et al 1987; 1990; 1991; Devore and Tucker 1988; Klonoff et al 1989; Rowley et al 1989; Strickland et al 1993; Daras et al 1994; Nolte et al 1996; Herning et al 1999; Broderick et al 2003). It is thought that cocaine induces a sudden rise in systemic arterial pressure, which precipitates vasospasm, endothelial disruption, disruption of cerebral autoregulation, with resultant intracranial hemorrhage, often in association with underlying aneurysms or arteriovenous malformations (Klonoff et al 1989; Levine et al 1991; Daras et al 1994; Konzen et al 1995; Fessler et al 1997). Indeed, chronic cocaine use appears to induce earlier clinical presentations in patients with incidental neurovascular abnormalities compared to similar non-cocaine users (Fessler et al 1997). Evidence for a true vasculitides is not compelling and most studies have failed to find any indication of vasculities, suggesting that the pathologic findings are a consequence of pharmacodynamic effects of cocaine and not a cocaine-induced vasculopathy (Nolte and Gelmann 1989; Nolte et al 1996). There is also a significantly increased risk of ischemic changes in the cerebral white matter and insular subcortex white matter (Bartzokis et al 1999a; 1999b). In some cases, vascular imaging and histopathologic studies suggest vasospasm of large arteries produced secondary intravascular thrombosis (Konzen et al 1995). Cocaine administration is associated with dose-dependent global and regional reductions in brain blood flow (Wallace et al 1996; Johnson et al 1998a), likely due to an immediate and brief period of vasoconstriction or vasospasm (Strickland et al 1993; Konzen et al 1995; Herning et al 1999). Cocaine-induced vasospasm can be partially blocked with calcium channel antagonists (Johnson et al 1998b; 2001). Chronic cocaine use can produce sustained brain perfusion deficit and persistent neuropsychological changes with deficits in attention, concentration, new learning, visual and verbal memory, word production, and visual-motor integration (Strickland et al 1993). Other manifestations of cerebral ischemia can result from direct embolization of foreign material injected with the drug diluents; mycotic aneurysms; as well as primary cardiac problems, including cardiac arrest (even in young patients), cardiac arrhythmias, cardiomyopathy with associated atrial or ventricular thrombus, aortic dissection, and endocarditis resulting from intravenous drug abuse (Kaku and Lowenstein 1990; Petty et al 1990; Sauer 1991; Sloan and Mattioni 1992; Moliterno et al 1994; Hollander 1995; Neiman et al 2000; Lange and Hillis 2001; Lange et al 2001; Kloner and Rezkalla 2003; Bolouri and Small 2004). Cocaine use during pregnancy can produce fetal hypoxia, intracerebral hemorrhage, and congenital malformations (Heier et al 1991; Brown et al 1992; King et al 1995). In a retrospective case-control study, maternal cocaine use was significantly associated with increased risks of neonatal stroke and congenital malformations (particularly neural tube defects), attributed to cocaine-induced vasospasm in the third and first trimesters, respectively (Heier et al 1991). Transcranial Doppler ultrasound studies of newborns who were exposed to cocaine in utero demonstrate increased flow velocities in intracranial arteries consistent with the vasoconstrictive effects of cocaine (King et al 1995). The mechanisms of cocaine-related cerebrovascular disease remain somewhat controversial, with several explanations proposed with varying degrees of support from human studies and animal models (Muir and Eliis 1993; Daras et al 1994; Kosten 1998; Buttner et al 2003; Fandino et al 2003). Proposed pathophysiologic contributors (not necessarily mutually exclusive) include pharmacologically-induced vasospasm, rapid transient increases in systemic blood pressure, disruption of cerebrovascular autoregulation (particularly with increasing levels of acute or hyperacute hypertension), impaired endothelium-dependent vasorelaxation, apoptosis of cerebral vascular muscle cells, arteritis, myocardial infarction with cardiac arrhythmias, impaired hemostatis, increased platelet aggregation, decreased global and regional cerebral blood flow, and cocaine-induced cerebral excitotoxicity (Kelley et al 1993; Muir and Ellis 1993; Daras et al 1994; Havranek et al 1996; Heesch et al 2000; Buttner et al 2003; Fandino et al 2003; Su et al 2003; Bolouri and Small 2004). Cocaine-induced vasospasm is thought to be mediated by endothelin-1, an extremely potent, 21-amino acid vasoconstrictor peptide produced by vascular endothelial cells; endothelin receptor antagonists can block cocaine-induced vasospasm in animal models (Fandino et al 2003). Cerebral vascular smooth muscle cells can undergo rapid apoptosis in response to cocaine, which may contribute to cerebral microvascular damage and strokes (Su et al 2003). In addition, work in animal models suggests that some of the adverse neurologic complications of cocaine use are medicated by changes in calcium or magnesium concentrations in vascular smooth muscle cells or brain, including precipitation of cerebral vasospasm by rapid elevation of intracellular free calcium and depletion of magnesium in vascular smooth muscle cells (Altura and Gupta 1992; Altura et al 1993; 1997; Zhang et al 1996). Amphetamine and derivatives, including methamphetamine and "ecstasy." Amphetamine is another potent sympathomimetic drug that can cause a wide variety of vascular complications, including stroke, aneurismal rupture, and myocardial infarction, similar to the case with cocaine (Chen et al 2003). Methamphetamine (aka: meth, crystal, speed) is a derivative of amphetamine that also acts as a CNS stimulant. Amphetamine and methamphetamine are administered in several ways (eg, orally, or by injection, smoking, or snorting). Prolonged use at high levels can produce dependence. Methamphetamine was widely used clinically in the 1950s and 1960s for treatment of depression and obesity (Anglin et al 2000). Until the late 1980s, methamphetamine use was endemic in California and relatively restricted to that state, but use has subsequently broadened with increased use, particularly in the Midwest (Anglin et al 2000). Approximately 2% of the US population have tried methamphetamine at some point in their lives. "Ecstasy" and "eve" are newer drugs of abuse, being ring-substituted amphetamines (3,4-methylenedioxymethyl-amphetamine, or MDMA, and 3,4-methylenedioxyethylamphetamine, or MDEA, respectively) that have greatly increased in popularity in the United States in the last decade. Neurologic and psychiatric complications of amphetamine, methamphetamine, and other amphetamine derivatives are similar to those seen with cocaine, and include ischemic and hemorrhagic strokes, anxiety, paranoia, hallucinations, and insomnia (Lambrecht et al 1993; Perez et al 1999). In some cases, intracranial hemorrhage occurs in the setting of underlying vascular malformations (Auer et al 2002). Pathological studies have suggested multiple pathophysiological mechanisms of brain and other organ damage, including perivascular hemorrhagic and hypoxic changes similar to those of heat stroke and other forms of hyperthermia (Milroy et al 1996). References: Altura BM, Gebrewold A, Altura BT, Gupta ARK. Magnesium protects against cocaine-indiced hemorrhagic stroke in a rat model: a 31P-NMR in-vivo study. Front Biosci 1997;15:a9-12. Altura BM, Gupta RK. Cocaine induces intracellular free Mg deficit, ischemia and stroke as observed by in-vivo 31P-NMR of the brain. Biochim Biophys Acta 1992;1111:271-4. Altura BM, Zhang A, Cheng TP, Altura BT. Cocaine induces rapid loss of intracellular free Mg2+ in cerebral vascular smooth muscle cells. Eur J Pharmacol 1993;246:299-301. Anglin MD, Burke C, Perrochet B, Stamper E, Dawud-Noursi S. History of the methamphetamine problem. J Psychoactive Drugs 2000;32:137-41. Auer J, Berent R, Weber T, Lassnig E, Eber B. Subarachnoid hemorrhage with "Ecastsy" abuse in a young adult. Neurol Sci 2002;23:199-201. Baquero M, Alfaro A. Progressive bleeding in spontaneous thalamic hemorrhage. Neurologia 1993;9:364-7. Bartzokis G, Beckson, Hance DB, et al. Magnetic resonance imaging evidence of "silent" cerebrovascular toxicity in cocaine dependence. Biol Psychiatry 1999b;45:1203-11. Bartzokis G, Goldstein IB, Hance DB, et al. The incidence of T2-weighted MR imaging signal abnormalies in the brain of cocaine-dependent patients is age-related and region-specific. AJNR Am J Neuroradiol 1999a;20:1628-35. Bolouri MR, Small GA. Neuroimaging of hypoxia and cocaine-induced hippocampal stroke. J Neuroimaging 2004;14:290-1. Broderick JP, Viscoli CM, Brott T, et al. Major risk factors for aneurismal subarachnoid hemorrhage in the young are modifiable. Stroke 2003;34:1375-81. Buttner A, Mall G, Penning R, Sachs H, Weis S. The neuropathology of cocaine abuse. Leg Med 2003;(5 Suppl 1):S240-2. Chen HJ, Liang CL, Lu K, Liu CC. Rapidly growing internal carotid artery aneurysm after amphetamine abuse: case report. Am J Forensic Med Pathol 2003;24:32-4. Daras M, Tuchman AJ, Koppel BS, Samkoff LM, Weitzner I, Marc K. Neurovascular complications of cocaine. Acta Neurol Scand 1994;90:124-9. Devore RA, Tucker HM. Dysphagia and dysarthria as a result of cocaine abuse. Otolaryngol Head Neck Surg 1988;98:174-5.