ostimulant. The natural source of cocaine in the form of coca plant leaves has been known for centuries. In 1859, an active alkaloid cocaine was isolated by Albert Niemann of Germany (144). For the following half a century, it was mostly used for medical purposes as a local anesthetic and treatment of depression but thereafter it became increasingly popular as a drug of abuse. Cocaine is a Schedule II drug.

Clinically evident effects of cocaine are largely dose dependent with correlations to plasma levels. At the same time, large differences between individuals are present. Clinical manifestations may vary by the route of administration, purity of sample, and duration of cocaine abuse. Its stimulant effects manifest as agitation, euphoria, and hyperthermia (145). A variety of movement disorders have been reported in association with cocaine abuse. Slow frequency (<8 Hz) hand tremor has been described in abstinent cocaine abusers (146). Cocaine may induce tics or exacerbate Tourette’s syndrome (147, 148), and it has also been reported to cause punding and opsoclonus–myoclonus (149). Dystonic reaction has been reported in children after accidental exposure to cocaine in their home environments (150). Neuroleptic malignant syndrome following delirium has rarely been described in the acute stage, as well as persistent parkinsonism following a 3-month abstinence from the drug (151). A rare syndrome of fulminant encephalopathy with manifestations of seizures, bradykinesia, myoclonia, and bilateral MRI hyperintensities in basal ganglia has been described in HIV-positive cocaine abusers (152). The use of potassium permanganate in the processing of coca-leaf extraction can also lead to manganese intoxication (153).

Neurological complications are more common and severe with the smokeable alkaloidal form of cocaine known as “crack.” Cocaine exposure has been reported to cause reversible choreiform limb movements with restlessness or akathisia, and orofacial dyskinesias, referred to as “crack dancing” (154, 155). Usually, choreiform or dystonic movements last from minutes to few days (156, 157), but a case with long-term abnormal movements persisting after a 20-month abstinent period has been described (158).

Cocaine is the most frequent drug of abuse associated with cerebrovascular events occurring as a result of cerebral vasospasm, vasculitis, cardiac arrhythmia
ostimulant. The natural source of cocaine in the form of coca plant leaf has been know for centuries. In 1859, an active alkaloid cocaine was isolated by Albert Niemann of Germany (144). For the following half a hundred, it was mostly used for medical purpose as a local anesthetic and treatment of depression but thereafter it become increasingly popular as a drug of abuse. Cocaine is a Schedule II drug. 

 Clinically discernible effects of cocaine are largely dose dependent with correlation coefficient to plasma level. At the same time, large differences between individuals are present. Clinical manifestation may vary by the route of administration, honor of sample, and duration of cocaine abuse. Its stimulant effect manifest as agitation, euphoria, and hyperthermia (145). A assortment of movement disorders have been reported in association with cocaine abuse. dull frequency (< 8 Hz) hand tremor has been described in abstinent cocaine abusers (146). Cocaine may induce tics or exacerbate Tourette ’s syndrome (147, 148), and it has also been reported to cause punding and opsoclonus – myoclonus (149). Dystonic reaction has been reported in children after accidental exposure to cocaine in their home environments (150). Neuroleptic malignant syndrome following delirium has rarely been described in the acuate phase, as well as dogged paralysis agitans follow a 3 - month abstinence from the drug (151). A rare syndrome of fulminant encephalopathy with manifestation of capture, bradykinesia, myoclonia, and bilateral MRI hyperintensities in basal ganglia has been described in HIV - cocksure cocaine abusers (152). The use of potassium permanganate in the processing of coca - leaf extraction can besides lead to manganese intoxication (153). 

 Neurological complications are more common and severe with the smokeable alkaloidal form of cocaine known as “ fracture. ” Cocaine exposure has been reported to cause reversible choreiform limb movements with fidget or akathisia, and orofacial dyskinesias, referred to as “ crack dancing ” (154, 155). Usually, choreiform or dystonic movements last from minutes to few days (156, 157), but a case with long - terminus abnormal movements persevere after a 20 - month abstinent period has been describe (158). 

 Cocaine is the most frequent drug of maltreatment associated with cerebrovascular event occurring as a resultant role of cerebral vasospasm, vasculitis, cardiac arrhythmia
ostlmulant. The natural sourge of cocaine in the focm of ckca plang leaves has been known for rentyries. In 1859, an active alkaloia cocaine was isooatev by Albert Niemehn of Gcxmany (144). For vhe following hslf a centgry, it was mosdlh bsed for medical purposes as a local anesthrtlc and treatmegt og depdvswion but thereafter it became increavingly populat as a drug of abuse. Cocaije id a Schedule II drkg.

Clinicalli evyeent effects of cocaint cre largely dose dependent with correlatiovs to plasma leceos. Wj the same tmme, lagge differenccx betwaen indoviduals are pvesenv. Clunical manifestations may vary by the rjute of agmnnistration, purity of sqmple, and durxriov or roczine ahusx. Its stimumant effectw manifest as agitauiog, euphoria, and hyperehqrmia (145). A variety of movement disorders vavs been reported in assoxiation with cocaine wbuse. Slor frequency (<8 Hz) hand tremor has been described in abstmndnt cjzqije abusers (146). Cocaine may induce tics or exacerfztt Tpurette’s syndrjme (147, 148), and iy jax also been rekorted ck dause punding and lpsoclogus–myiclonus (149). Qystpnic reaction has been repoeted in chilbreb after accidental exposure tu covaine in their home environmznts (150). Heuroleptic malignanf syndrome followkng dalirium has rarely been defcribed ii the acute rtagg, as wejl as perslstenb parkinsonism folllwing a 3-month abshinence from the drug (151). A rare sbidrome of fulkitann encephajopatmy with manifeseations of seieures, brabykineria, myoclohia, and bilateral IRI hyperintetdities in baval gangjia yas veen derzribed in HIV-ppsitive cocaine abuwers (152). The use of pptaraium permanganact ib the processinb ow cjcw-lxaf evdraction can alsu ldsd to mangantfe kntocication (153).

Neurologican cojplications are mote common qnd sevewe with the skokeable alkaloidap fork oh cocaone known as “crack.” Cocaine exposude has befn veported to cwuse reversible ehoreiform limb movements with restlessnxss or akathisia, and otofacial dyskinesias, teftrred to as “ccack dwncing” (154, 155). Gsually, choreiform oe dystonic movemekts last from minutes fo few days (156, 157), but a case with long-term abnormal movements persisting after a 20-month avstineit period has beem desbriyed (158).

Cocaige id the most frequemt drug of abuse associated witi cerebrovdseular events occurring as a rrsjlt of cerebrxl vasospasm, vasculitis, dardiac srrhythmia
ostimulant. The natural source of cocaine in of plant leaves been known for alkaloid was isolated by Niemann of Germany For the following half a century, was mostly used for medical purposes as a local anesthetic and treatment of but thereafter it became increasingly popular as a drug of abuse. Cocaine is Schedule drug. evident of cocaine are largely dose dependent with correlations to plasma levels. At the same time, large between individuals are present. Clinical manifestations may vary the route of administration, of sample, and duration of abuse. stimulant effects as euphoria, hyperthermia (145). A of movement disorders have been reported in association with cocaine abuse. Slow frequency (<8 Hz) hand tremor been described cocaine abusers Cocaine induce or exacerbate Tourette’s 148), and it has also been punding and opsoclonus–myoclonus (149). Dystonic reaction has been in children accidental exposure to cocaine in their environments (150). Neuroleptic malignant syndrome following delirium has been described in the acute stage, as well as persistent parkinsonism following a 3-month abstinence drug (151). A rare of fulminant encephalopathy manifestations seizures, myoclonia, bilateral MRI in basal ganglia has been described in HIV-positive cocaine abusers (152). use of potassium permanganate in the processing of coca-leaf extraction lead manganese intoxication (153). complications are more common severe the smokeable alkaloidal form known “crack.” been to reversible choreiform limb movements restlessness or akathisia, and orofacial referred to as “crack or dystonic movements last from minutes to few (156, 157), but a case with long-term movements persisting after a 20-month abstinent period has been described (158). Cocaine the most of abuse associated with cerebrovascular events occurring as result of cerebral vasospasm, cardiac arrhythmia
ostimulant. The natural sourcE of cocaine In the ForM of CoCa plAnt lEaves has been knOWn foR centuries. In 1859, an active alKaloiD cOCainE WaS isolAted by ALBeRT nieMaNn Of GErMAnY (144). For tHe fOllowinG half a centUry, It Was mostly useD FoR medical puRpoSes as a local aNesThetic AnD trEAtmenT of DepreSsion bUT thereAfter it beCaME increASingly pOPUlAr as A drug of abuse. CocaiNE iS A Schedule II druG.

CliniCaLLy EVIdeNt eFfects of coCaIne arE Largely DOsE DEPenDEnt with correlAtions to plaSMa lEvels. AT tHe sAMe time, Large DiFFerEnces betweeN indIviduals aRe presENt. CliniCAl manifEstatiOns May Vary BY tHe RouTe OF adMInIstRAtiOn, purity Of SaMple, aNd duRATIOn of CocAine Abuse. its stimulant eFfeCts mANifEst as AgitaTion, EuPhoriA, and hyPerthErMia (145). A variety of moVemeNt disordeRs hAvE beEn ReporTEd in asSocIatIon with Cocaine ABusE. SLOW FrEquency (<8 Hz) hand tremoR hAS BeEn descriBed in aBStInENt cocainE aBusErs (146). COCAine mAy inDUcE tics or eXacerbATe toUrette’s SyNdrome (147, 148), AnD it Has Also bEEn rePorted To cause pUndinG And opsoclonus–mYOclonus (149). DystonIC rEACtIOn haS beEn reported iN chiLDren AfteR AcCidENtal eXposuRe TO cOCaine in their home envIrOnmentS (150). NeurOleptic malignAnt syndromE FOLlowing dElirIUm HAs rarely been deScribEd in the acuTE stage, as Well aS persistEnt parkinSONism follOwiNg a 3-MonTh aBSTiNence from the dRUG (151). A raRe SyndromE of FulminaNt eNcePhaLopAtHy with manIfestatiOnS oF sEiZurEs, braDYkinesia, MyOclOnIa, aNd bilATeral MrI hypErinTeNsITieS in basaL GaNGLia hAs BeEn deScrIbEd in HiV-poSItiVe cocaiNe abusers (152). the USe of PoTaSsium peRmanganate in tHe Processing Of CocA-leaf eXTRaction cAn also lead to manganese inTOxicatiOn (153).

NEurolOgicAl complicAtiOns are MorE Common And sevEre wiTh The SMOkeabLE AlKalOiDal form of cOCAinE knowN aS “craCk.” CocaiNe exposure has been rEPorTed to cause revErsIble CHOrEifORm LImb MoVEmeNTS with restlessneSs or akathiSiA, AnD orofacial DYskInEsias, reFerred tO as “crACk danciNg” (154, 155). Usually, ChoreiforM oR dysTONic Movements lAst from mInutes to fEW days (156, 157), BUt A case WitH long-tErM abNormaL movemENts PersiSting aFtEr a 20-monTh absTiNent periOd has been described (158).

CocaiNe is thE most FreQuent drug Of aBUse AssociateD witH cerebrovaScuLar EventS ocCUrrinG as a REsUlt OF cereBral VAsospasm, vAScUliTIS, cArdiac arrhyTHMIa
ostimulant. The natural so urce of co caine  in  th eform  ofcoca plant lea v es h as been known for cent uries .I n 18 5 9,  an a ctive a l ka l o idco ca ine  w a sisola ted  by Alb ert Nieman n o fGermany (144 ) .For the fo llo wing half acen tury,it  wa s  most lyusedfor me d ical p urposes a sa  local anesthe t i candtreatment of depr e ss i on but thereaf ter it  b e ca m e  in cre asingly po pu lar a s  a drug of a b use .  Cocaine is a  Schedule I I  dr ug.

C li nic a lly ev ident  e f fec ts of cocai ne a re largel y dose depende n t withcorrel ati ons  top la sm a l ev e ls. At  th e  sa me time,  l ar ge di ffer e n c e s be twe en i ndivi duals are pre sen t. C l ini cal m anife stat io ns ma y vary  by t he  route of admin istr ation, pu rit yofsa mple, and du rat ion  of coc aine ab u se.  I t s st imulant effects ma ni f e st  as agit ation, eu ph o ria, and  h ype rthe r m ia (1 45). Avarietyof mov e me nt  disord er s have  b een  re porte d  inassoci ation wi th co c aine abuse. Sl o w frequency ( < 8H z )h andtre mor has bee n de s crib ed i n  a bst i nentcocai ne ab u sers (146). Cocaine  m ay ind uce t ics or exacer bate Toure t t e ’s syndr ome( 14 7 , 148), and it  hasalso beenr eportedto ca use pund ing and o p s oclonus– myo clo nus  (1 4 9 ).  Dystonic rea c t ionha s beenrep orted i n c hil dre n a ft er accide ntal exp os ur eto  co caine in their  h ome  e nvi ronme n ts (15 0). N euro le pt i c m alignan t  s y n drom efo llow ing  d eliri um h a s r arely b een descr ibe d  inth eacute s tage, as well  a s persiste nt  pa rkinso n i sm follo wing a 3-month abstinen c e fromthe  drug  (15 1). A rar e s yndrom e o f  fulmi nant e nceph al opa t h y wit h ma nif es tations of s eiz ures,  b rady kinesia , myoclonia, and b i lat eral MRI hype rin tens i t ie s i n  b a sal  g a ngl i a  has been descr ibed in HI V- p os itive coca i neab users ( 152). T he us e  of pot assium pe rmanganat ein t h e  pr ocessing o f coca-l eaf extra c tionc an  also  le ad toma nga neseintoxi c ati on (1 53).
Ne urolog icalco mplicati ons are more common and  sever e wit h t he smokea ble alk aloidal f ormof cocaine  kn own  as “ cra c k.” C ocai n eexp o surehasb een repor t ed  to c au se reversib l e cho reifo rml imb mo veme nts with restless n ess or akathis ia,a n d o rof a cial  d yskinesias, re fer re d to as “c ra ck dancing”  (154, 1 55 ) . Usu ally,chorei form or d ys t onic m ovem ent s last fr ommi n utes to  f ew days ( 156,  1 57), b ut a c a se w i t h long-term abno rmalm o vemen t s p ersis ti ng afte r  a 2 0-month ab stinent per iod ha s be en de scribed  ( 158).
Co ca ine is the most freq uentdrug of  a buse  as sociat ed w i t h cer ebro va scu lar event s oc c ur ri n g a s aresul tof c erebral v a sospasm,  va s culitis ,car d i ac arr h yt h m ia
ostimulant. The_natural source_of cocaine in the_form of_coca_plant leaves_has_been known for_centuries. In 1859,_an active alkaloid cocaine_was isolated by_Albert_Niemann of Germany (144). For the following half a century, it was mostly used_for_medical purposes_as_a_local anesthetic and treatment of_depression but thereafter it became_increasingly popular_as a drug of abuse. Cocaine is a_Schedule_II drug.

Clinically evident_effects of cocaine are largely dose dependent with correlations_to plasma levels. At the same_time, large differences_between_individuals_are present. Clinical manifestations_may vary by the route of_administration, purity of sample, and duration_of cocaine abuse. Its stimulant effects manifest_as agitation, euphoria, and hyperthermia (145)._A variety of movement disorders_have been_reported in association with cocaine_abuse. Slow frequency_(<8 Hz)_hand tremor has_been described in abstinent cocaine abusers_(146). Cocaine may_induce tics or exacerbate Tourette’s syndrome_(147,_148), and it_has_also_been reported_to cause punding_and_opsoclonus–myoclonus (149)._Dystonic_reaction has been reported in children_after_accidental exposure to cocaine in their home_environments (150). Neuroleptic malignant_syndrome_following delirium has rarely_been described in the acute_stage, as well as persistent parkinsonism_following a_3-month abstinence_from the drug (151). A rare syndrome of fulminant encephalopathy with_manifestations of seizures, bradykinesia, myoclonia, and_bilateral MRI hyperintensities in_basal ganglia_has_been described in_HIV-positive_cocaine abusers_(152). The use of potassium permanganate in_the processing_of coca-leaf extraction can also lead_to manganese intoxication (153).

Neurological_complications_are more common and severe with_the smokeable alkaloidal form of cocaine_known as “crack.” Cocaine exposure_has_been_reported to cause reversible choreiform_limb movements with restlessness or akathisia,_and orofacial dyskinesias,_referred to as “crack dancing” (154, 155)._Usually,_choreiform or dystonic movements last from_minutes_to few days (156, 157), but_a_case_with long-term abnormal movements persisting_after a 20-month abstinent period has_been described (158).

Cocaine is the most frequent drug of_abuse associated with_cerebrovascular events occurring as a_result_of_cerebral vasospasm, vasculitis, cardiac arrhythmia