Brain structural -haemodinamic changes caused by Methcathinone (Ephedron) abuse. Brain structural -haemodinamic changes caused by Methcathinone (Ephedron)

Brain structural -haemodinamic changes caused by Methcathinone (Ephedron) abuse.

D. Gachechiladze, , F. Todua, M.Okujava , D. Miminoshvili

Research Institute of Clinical Medicine

Tbilisi, Georgia

Poster #: EP-37

Poster #: EP-37

Title: Methcathinone (Ephedron) abuse- Brain structural -haemodinamic changes

Disclosure Statement: No disclosures

Toxic encephalopathy, also known as toxic-metabolic encephalopathy, is a degenerative neurologic disorder caused by administration of toxic substances, that can be presented with different neurological abnormalities.

85%

15%

Encephalopathy Toxic encephalopathy

PURPOSE:

The aim of our study was to assess the neuroradiologic and haemodinamic findings in patients using synthetic (self-made) manganese based psychoactive substances (Methcathinone).

Ephedrone - derived via the oxidation of Ephedrine (pseudoephedrine) + potassium permanganate + acetyl salicylic acid (aspirin)

Street names – “Cat”, “Jeff”, “Speed”, “Russian Cocktail”

Psychoactive substance

The duration of the substance abuse ranged from 7 month to 7 years.

Patients age ranged from 23 to 54 years

2007-2013 years were investigated 41 patients (35 male and 6 female) with chronic intravenous use of manganese based drugs.

Materials and Methods:M

Materials and methods

Collor Doppler of extra-intracranial vessels Toshiba Aplio 500, AplioXG

MRT, MRA- Siemens Magnetom Avanto (1.5T), Magnetom Aera (1.5T), Siemens Magnetom Verio (3T)

T1(se)-TR -570 ms, T1(fl) - TR -31 ms, T2(se)-TR -6000 ms, TE-118ms – pulse sequences

2 cases- MSCT / CTA- Siemens Somatom Definition Edge(384sl) Toshiba Aquilion One 640sl.

Mn accumulation depletes dopaminergic systems and causes some neurological symptoms.

Toxic encephalopathy is attributed to manganese induced oxidative stress. High concentration of the proteins transform the Mn2+ into Mn3+, which is

highly toxic and inhibites mitochondrial activity.

Euphoria Hyperactivity (mostly without any reason) Logorrhea (mostly without any meaning) Increase libido Impulsiveness Tachicardia Parestesis

after 4-6 hours Headache, Apathy, Depression

Memory impairment (verbal and non-verbal. Irrational thinking. Personality changes :Aggressive ,Obsessive, Destructive

Substance abuse with the duration of more than 6 months was associated with stabile neurological disabilities.

Most patients had the combination of extrapyramid disorders (parkinsonism, muscular dystonia, tremor, myoclonia) with mild cognitive abnormalities (bradyphrenia, attenuated attention, reduced working capacity, decreased phonetc verbal fluency, tendency to impulsivness).

Parkinsonian syndrome (Manganism)

Medications used for treatment of Parkinson’s disease are less effective.

Bradykinesia OligokinesiaBradymimia (mask-like face)TremorDystonia of the lower extremities

Retro and Anteropulse

“Cock-walk”gait in which patients walk on their toes, feet not comletely contacting with the ground.

(there is tendency to fall while walking backwards).

“Cock-walk” gait

Abnormalities were revealed in 35 (85%) cases

0%

20%

40%

60%

80% 75%

56%69%

15%9%

Characteristic lesions are revealed on MR T1-weighted images. Hyperintense signals detect on the different structures of brain, most common on the

level of globus pallidum.

The MRI signal abnormalities e caused by the accumulation of manganese.

The signal intensity was higher after recent and frequent use of the drug, but changes were not associated with the clinical pictures.

T1-weighted Hyperintense signals

In cases of the termination of the substance use, pathologic signal in basal ganglia disappeared after 6-8 months, but clinical signs remained unchanged.

41y. Old male. Abuse 2.5y. Stroke. Thrombosis of left MCA-M2

MDCTA

CTP

TCCD

27Y. Male. Abuse 3y. Spontaneous dissection of the left ICA.

Tof-fl-2d-MIP

Same patient

TCCD T2 tirm tra dark-f ep 2d diff orth p2

0

20

40

60

80

100

120

V sis V mean V dia

A-MCA

C-MCA

A-MCA

C-ACA

Mean, sistolic and diastolic flow for abusers (A) and control (C) subjects.

Tof-fl-3d-MIP

Vessel irregularity ( vasoconstrictiom / vasodilatation) – 28 (67%) cases;

0

0,2

0,4

0,6

0,8

1

MCA ACA

Abuse

Control

Pulsation indexes (PI) for abusers and control subjects

BHI (%)= (MFVap-MFVrest)x 100 /MFVrest x30

Abuse Women 0.87± 0.53 Abuse Men 0.72± 0.41

Healthy 0.97± 0.44

Our results suggests, that MRI demonstrate systematic brain structural changes in Methcathinone abusers. Slowed cerebral blood flow velocity with increased pulsatility and impaired CRV in abusers indicate increased cerebrovascular resistance due to vasoconstriction of small cortical vessels.

Neurovisualisation play important role in detection and differentiation of brain abnormalities in patients with drug abuse history and therefore in selection of adequate treatment tactics.

CONCLUSION

Thank you for attention