Hypoxia and Medicine

Cardiac ischemia? What causes Cardiac ischemia?

How are cardiac ischemia and shortness of breath related? I have had significant shortness of breath and am being treated with inhalers, nebulizer and meds. EKG and chemical stress test results said "provocable ischemia of interior (anterior?) wall ". Haven't gotten results of echocardiogram yet. I had it done 3 weeks ago, shouldn't I have heard something from my PCP by now whether it be good or bad? I am scheduled to see a cardiologist next week. Am I to assume that cardiologist will read echo before I am to see him and that is the way I will get the results?

How is ST elevation/depression measured? How much indicates cardiac ischemia? When doing EKG monitoring, how much ST depression or elevation indicates that the myocardium is ischemic?

Why use CKMB andTroponin for assessment of Cardiac Ischemia?

how much is a cardiac stress test ? the test where you get on a treadmill and the doctor checks your heart for signs of ischemia, disease, etc... I can't everything is closed untill Monday, and I need to know today, at least give me a rough estimate, thanks.

Can Summarize the discussion for me please? We have demonstrated for the first time that inhalation of common air pollutants affects the systemic vasculature of humans. Short-term exposure to PM2.5 and O3 at levels that occur in urban environments causes acute conduit artery vasoconstriction without producing immediate alterations in endothelial-dependent or -independent vasomotion. This finding is important because it suggests that alterations in arterial tone may be a relevant mechanism contributing to air pollution–mediated acute cardiac events and because it provides evidence that the observations shown by large epidemiological studies are biologically plausible.1 Relevance of Conduit Artery Vasoconstriction It is reasonable to suspect that the coronary vasculature may respond similarly to air pollution exposure because brachial and coronary reactivity strongly correlate (r=0.79, P<0.001 for brachial versus coronary FMD).10 Even so, a reduction in coronary diameter of this relatively small magnitude (0.1 mm) would have minimal impact on healthy adults. However, congruent with epidemiological findings that individuals at increased risk for acute air pollution–related cardiac events generally have pre-existing cardiovascular disease, 2 this degree of sudden coronary vasoconstriction could promote cardiac ischemia in those with underlying flow-limiting obstructive lesions or could trigger instability of susceptible plaques.11 Furthermore, the vasculature of patients with coronary risk factors is known to hyper-react to a variety of vasoconstrictors,12,13 which potentially increases their susceptibility for acute cardiac events after air pollution exposure. Additional investigations in the coronary circulation and in high-risk individuals are needed to confirm these hypotheses. Mechanisms and Mediators of Vasoconstriction Because this is the first study to investigate the effects of air pollution on the vasculature, a more complete understanding of the pathophysiological mechanisms underlying our observations and the specific pollutants involved requires further investigation. Substantial evidence links increased PM2.5 alone with cardiac mortality.1 However, our initial air pollution exposure was chosen to be PM2.5 plus O3 because this mixture occurs in "real-life" settings. At present, an effect on the vasculature partially mediated by O3 cannot be ruled out. Determinations of the relative importance of PM2.5 versus O3 and specific components in fine particulate matter await follow-up studies now that a meaningful effect of urban air pollution on vascular function has been demonstrated. Potential biological mechanisms for the vasoconstriction include a reflex increase in sympathetic nervous system activity via stimulation of pulmonary vagal afferents14 or an acute increase in vascular ET release, analogous to cigarette smoking.15 PM2.5 inhalation has been shown to induce systemic inflammation and cytokine production,16 possibly related to free radical activity of components in particulate matter.17 In turn, these have the capacity to enhance vascular ET expression by direct mechanisms or via activation of oxidative stress pathways.6 Indeed, we have previously demonstrated the presence of increased plasma ET levels acutely after PM2.5 exposure.5 In conclusion, alterations in arterial tone and reactivity in response to PM2.5 and O3 exposure is a new arena for future research into the biological mechanisms linking air pollution with acute and potentially chronic cardiovascular events. Further investigations are needed to confirm and extend our findings to the coronary circulation and to subjects with existing heart disease.

can someone help me please? my grandmother has cardiac ischemia can someone here tell me more about this condition.

PLEASE help me understand my heart tests (I am confused!!!)? I am a 36 year old male (non-smoker) that had an abnormal Echocardiogram and stress test 2 months ago. Here were the results: 1) Echocardiogram: Mild Hypokinesis of base and mid septum. Ejection Fraction of 55%. 2) Exercise Stress Test: Anterior and inferior ischemia. Normal Electrocardiogram response. Ejection Fraction of 45%. At that point the Cardiologist was sure that I had blockages so I underwent a Cardiac Catheterization the following day. The results were normal coronary arteries. Normal left ventricular function with no wall motion abnormalities. Ejection Fraction of 50%. No blockages. No underlying disease. The cardiologist actually told me that my arteries were so clear that he could "ski" through them. The only explanation that he could give me for the abnormal Echo and stress test were that they were "FALSE POSITIVES". I am a bodybuilder and he stated that my larger chest size could have possibly given inaccurate readings on these types of tests. The only medications that he has me on are Lisinopril for slightly elevated blood pressure and Lipitor for slightly elevated cholesterol. Otherwise, he sent me home with no restrictions. He stated that my heart is just "slightly" weaker than normal but that I can improve it with aerobic exercise and good blood pressure/cholesterol control. He did not seem concerned in the least. Have you guys ever heard of having "false positives" on the above tests and then being cleared with the heart cath? I have been stressing over this for the past 2 months.

Is there a cure for Atrial Fibrillation and Left Bundle Branch Block? Throughout most of my adult life, I have had "palpitations". I had EKGs and even wore a holter monitor about 14 years ago. Doctors just sort of ignored it. A few weeks ago, during a routine colonoscopy, the LBBB was discovered. I then had an EKG, ECHO and Stress test that indicated ischemia. Cardiologist recommended a cardiac cath which was done on Monday. But while in the hospital on monitor, I went into A-Fib. So, for the first time, the "palpitations" I have had several times a year were recorded and diagnosed as A-FIB. The cath was clear, no blockages in the arteries. I was sent home on Lopressor and baby aspirin. I do not have high cholesterol or high blood pressure. Now I am having multiple A Fibs a day and feel light headed. Can I stop taking the Lopressor? Is there another drug that will prevent it? Thanks for listening!!!

i have to make a case study on preeclampsia. below are the guidelines/examples.. pls help? I.Patient’s Profile General Data NameF.B. Age59 years old SexMale Civil StatusMarried OccupationHousewife History of Present Illness The patient has a known case of Rheumatic Heart Disease (RHD). Patient underwent Mitral Valve Repair (MVR) in 1999 and has been on Coumadin therapy with no regular follow up of bleeding parameters. Six days prior to admission, patient experienced headache and dizziness, but no consult was made. Instead, patient self-medicated with Bonamine which afforded relief. Three days prior to admission, headache persisted with increased severity, which prompted patient to seek medical assistance at FEU Hospital. Mobic and Iterax were given. Few hours prior to admission, patient was noted to have changes in sensorium and relatives decided to seek consult at Philippine Heart Center. Upon admission, patient was noted to be unresponsive, stuporous, and speechless, with GCS of 7 (E2V1M4). Past Medical History The patient has denies any history of Diabetes Mellitus and Hypertension. As mentioned, she had a history of Rheumatic Heart Disease and had Mitral Valve Repair in 1999. She is a non-smoker and non alcoholic drinker. Nursing Assessment (Problem-Based) Neurologic: LOC: drowsy to stuporous, 3-4 mm pupil size anisocoric, with brisk reaction to light; GCS – 9 (E4- Spontaneous eye opening V1- none/mechanical ventilation M4 – withdraws to pain) (+) doll’s eye reflex (+) babinski on right foot (-) corneal reflex, no visual threat Respiratory Patient is hooked to a mechanical ventilator through a tracheostomy. Ventilator set-up: 350/30/14/AC/5. (+) crackles on both lung fields. With equal breath sounds. Cardiac With atrial fibrillation; fine course, with occasional unifocal PVC’s. HR = 97 BP= 120’s-130’s/60’s-70’s. Musculo-Skeletal No contractures noted but there was stiffness noted at the right wrists and both ankle joints; with normal muscle tone and non-spontaneous movement; with severe weakness on both upper and lower extremities. Hematologic Latest PTPA: INR = 1.02 Act = 98% II.Anatomy and Physiology of the Brain Blood Supply of the Brain The blood supply of the brain derives from the aortic arch via the right innominate, left common carotid and left subclavian arteries. It includes the conducting and penetrating vessels. The venous system draining the brain is divided into vertebral veins that receive blood from the cerebellum. The cerebral veins have no valves. All the veins of the brain terminate into dural sinuses. External Brain Structures The brain is grossly divided into three main areas: the cerebrum, the brain stem and the cerebellum. The largest portion of the brain is the cerebrum. It consists of two hemispheres that are connected together at the corpus callosum. The cerebrum is often divided into five lobes that are responsible for different brain functions. The cerebrum’s surface—the neocortex—is convoluted into hundreds of folds. The neocortex is where all the higher brain functions take place. The cerebellum lies in the posterior fossa, separated from the cerebrum by tentorium cerebelli. It exerts ipsilateral control. It has three principal lobes. The Flocculonodular lobe is part of the vestibular system. It controls muscle tone, equilibrium and body position. The Anterior lobe receives most of the proprioreceptive and interoceptive input from head and body. It controls automatic movements and coordination. The posterior lobe coordinates voluntary movement. The ventricles The ventricles are a complex series of spaces and tunnels through the center of the brain. They secrete cerebrospinal fluid, which suspends the brain in the skull. They also provide a route for chemical messengers that are widely distributed through the central nervous system. Cerebrospinal fluid Cerebrospinal fluid (CSF) is a colorless liquid that bathes the brain and spine. It is formed within the ventricles of the brain, and it circulates throughout the central nervous system. It fills the ventricles and meninges, allowing the brain to “float” within the skull. The Meninges The meninges are layers of tissue that separate the skull and the brain. The Dura mater is the tough and fibrous membrane. The Arachnoid membrane is the delicate membrane and contains subarachnoid fluid. Pia mater is the vascular membrane. The subarachnoid space is fprmed by the arachnoid membrane and the pia mater. Normal Flow of Cerebrospinal Fluid Cerebrospinal fluid is produced in the Choroid plexuses of the ventricle. It flows from the lateral ventricles to the third ventricle passing through the interventricular foramen. Then it goes through the cerebral aqueduct to the fourth ventricle. From there fluid flows to the subarachnoid cisterns through the foramina of Magendie and Luschka to bathe the cerebral hemispheres. It exits through the saggital sinus to be absorbed by the arachnoid villi. III.Pathophysiology of Subarachnoid Hemorrhage (SAH) The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space between the pial and arachnoid membranes. SAH comprises half of spontaneous atraumatic intracranial hemorrhages, the other half consist of bleeding that occurs within the brain parenchyma. Intracranial hemorrhage as a whole comprises 20% of all strokes. Nontraumatic SAH usually is the result of a ruptured cerebral aneurysm or AVM. Blood extravasation into the subarachnoid space has a detrimental effect on both local and global brain function and leads to high morbidity and mortality rates. The classic clinical picture of SAH is marked by the onset of very severe headache, tagged as the “worst in life”. Other associated signs and symptoms are loss of consciousness, seizures, diplopia and focal neurologic signs. The early complications of SAH are rebleeding and hydrocephalus. Other complications include vasospasm, neurologic deficits, hypothalamic dysfunction and hyponatremia. Vasospasm from arterial smooth muscle contraction is symptomatic in 36% of patients. Neurologic deficits from cerebral ischemia peak at days 4-12. Hypothalamic dysfunction causes excessive sympathetic stimulation, which may lead to myocardial ischemia or labile detrimental BP. Hyponatremia may result from cerebral salt wasting (SIADH). Nosocomial pneumonia and other complications of critical care may occur. Pathophysiology Diagram Pathological Cycle Resulting from Increased Intracranial Pressure Surgical Treatment Ventriculo-peritoneal Shunting The ventriculo-peritoneal shunt diverts CSF from a lateral ventricle or the spinal subarachnoid space to the peritoneal cavity. A tube is passed from the lateral ventricle through an occipital burr-hole subcutaneously through the posterior aspect of neck and paraspinal region to the peritoneal cavity through a small incision in the right lower quadrant. IV.Nursing Diagnoses 1.Ineffective Breathing Pattern r/t neuromuscular impairment 2.Ineffective airway clearance related totracheobronchial secretions 3.Altered Level of Consciousness r/t decreased cerebral perfusion 4.Impaired Physical Mobility r/t neuromuscular impairment 5.Risk for Injury r/t possible shunt malfunction 6.Risk for Infection r/t post-surgical wound V.Discharge Care Plan (METHODS) MEDICATION •Reinforce importance of medication compliance to patient and her relatives; its time, frequency, duration dosage and route. •Advice to report unusual manifestations and side effects of drugs to physician. •Monitor and evaluate effectiveness of medication regimen. ENVIRONMENT/ EXERCISE •Instruct patients watcher to provide calm and non stressful environment to prevent stimuli that could lead to seizures and an increase in Intracranial Pressure •Advice to limit visitors •Provide environment within normal room and body temperature. •Maintain safe environment. •Institute seizure precaution. •Initiate positional precaution to prevent increase in intracranial pressure. •Teach patient’s relative to perform passive range of motion exercises on patient’s extremities. TREATMENT •Teach patient’s relatives proper shunt care. •Teach patient’s relatives how to suction properly. HEALTH TEACHING ON DISEASE PROCESS •Explain to patient’s relatives regarding patient’s neurological status and disease process, and its manifestations. •Discuss possible complications of VP Shunt and its signs and symptoms OUT PATIENT FOLLOW UP •Inform relatives regarding importance of compliance on follow-up check up. •In case of continued Coumadin therapy, stress the importance of regular PTPA monitoring. Diet •Refer to dietician for dietary instructions. SPIRITUAL / SEXUAL •Encourage patient’s relatives to seek spiritual support. •Encourage patient’s husband on alternative ways on showing affections such as hugs and kisses. XI.Bibliography Nolte, J. The Human Brain: An Introduction to Its Functional Anatomy, Fifth Edition., Mosby, 2002. ISBN: 0-323-01320-1 Stoler, D. Coping with Mild Traumatic Brain Injury, Avery Penguin Putnam, 1998. ISBN: 0895297914 Human Anatomy and Physiology, Fifth Edition., 2000. ISBN: 0805349898. Zuccarello, M. and McMahon, N. “Subarachnoid Hemorrhage”. www.mayfield.com, June 2004. Rinkel GJ, Prins NE, Algra A. “Outcome Of Aneurysmal Subarachnoid Hemorrhage In Patients On Anticoagulant Treatment.” www.pubmed.gov, August 28, 2000. Newton, Todd R., Subarachnoid Hemorrhage. Emedicine from WebMD. www.emedicine.com., December 19, 2005.

medical professionals..can u tell me what the results of this stress test means? 1-Quality control 180 degree rotational images show soft tissue attenuation anteriorly. There is no evidence of motion artifact seen on this study. 2- Review of the Spect images show hyperperfusion and anterior anteroseptal and apex which appears to be reversible when compared to resting images. This is suggestive of inducible ischemia in the anteroapical area. 3- Multigated cardiac wall motion study shows mild global hypokinesis with overall systolic function at the lower limit of normal. 4- Quantative evaluation of the left ventricular function shows end diastolic volume of 90 ml and systolic volume of 43 ml with calculated ejection fraction of 52%

Why do I get heart palpitations after eating? I already had a Cardiac cath (normal), thallium treadmill stress test (false/positive {recorded anterior apical ischemia}), ECG's (abnormal T waves and not conclusive of anything), echocardiogram (normal) and 48 hr holter monitor (14PVC's were recorded along w/ 44PAC's). Could exercising help improve palpitations? Could palpitations be caused by GERD? Doctor's say nothing is wrong w/ me. I am scheduled for Sleep Apnea Study.......I am so sick of this!!!!!

Can You Put This Inforamation Into Your Own Words & Short??? I Would Really Apprciate It ;)? Shock can be of four different types such as hypovlemic shock (low volume) due to decrease blood volume, cardiogenic shock due to poor heart function, vascular shock due to inappropriate vasodilation, and obstructive shock due tot eh obstruction of blood flow. A common cause of hypovolemic stock is acute (sudden) or hemorrhage. The blood loss may be external, as occurs in trauma , or internal, as in rupture of an aortic aneurysm. Loss of body fluids trough excessive sweating, diarrhea, or also vomiting also can cause hypovolemic shock. Other conditions – for instance, diabetes , mellitus- may cause excessive fluid of urine. Sometimes, hypovolemic shock is due to inadequate intake of fluid falls, venous return to the heart decline, filling of the hear lessens, stroke volume decreases, and cardiac output decreases. In cardiogenic shock, the heart fails to pump adequately, most often because of a myocardial infarction (heart attack). Other causes of cardiogenic shock include poor perfusion of the heart (ischemia), heart valve problems, excessive preload or afterload, impaired contractility of heart muscle fibers, and arrhythmias. Even with normal blood volume and cardiac output, shokc may occur if blood pressure drops due to a decrease in systemic vascular resistance. A variety of conditions can cause inappropriate dilation of arterioles or venules. In anaphylactic shock, a severe allergic reaction for example, to a bee sting- releases histamine and other mediators that cause vasodilation. In neurogenic shock, vasodilation may occur following trauma to the head that causes malfunction of the cardiovascular center in the medulla. Shock stemming from certain bacterial toxins that produce vasodilation is termed 100,00 deaths per year and is the most common cause of death in hospital critical care units. Obstructive shock occurs when blood flow through a portion of the circulation is blocked. The most common cause is pulmonary embolism, a blood clot lodged in a blood vessel of the lungs.

want is truth of the heart? Did pottle and nasir M.D. lied to me Letters from Susan Pottle and Shahid Nasir M.D. 12/17/2007? finding: aortic valve leaflets are mildly thickened. mitral valve: there is a trace of mitral regurgitation. tricuspid valve: there is trace tricuspid regurgitation prestent. right ventricular systolic pressure was measured at () mmhg. red blood cell count 4.42 is low, hemoglobin 12.7 is low, hematocrit 37.4 is low. EST GFR 42.6 is low. ALK PHOS 142 is high. Glucose 151 is high. Shahid Nasir M.D false stress and scan test finding mild ischemia involving the mid to apical portion of the inferior wall. and mild hypokinesis of the apical portion of the inferior wall. 1 day ago - 2 days left to answer. Additional Details 1 day ago Did pottle and nasir M.D. lied to me Letters from Susan Pottle and Shahid Nasir M.D. 12/17/2007? due to the fact that you were having chest pain, your physician, Dr. Kiwan, wanted you to have a muclear cardiac stress test. this exam is only a screening exam which shows if you have any defects within your heart; it is not necessarily the clearest method of visualizing your heart. if the test shows any abnormalities then the next test that you should have is a diagnostic coronary angiogram (aka heart catheterization), which you did have. fortunately, your angiogram showed that you did not have any problems with your heart. false positive results do occur in these test, that is why you were sent for the angiogram.

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.