Antipsikotik

Pengenalan

Antipsikotik adalah kelas ubat yang digunakan untuk merawat psikosis (penyakit mental yang menyebabkan
perubahan personaliti dan tidak peka dengan realiti).

Ubat-ubatan ini juga dikenali sebagai 'neuroleptik'.

Ubat-ubatan ini memberi kesan kepada sistem perhubungan khas yang membenarkan komunikasi antara
sel-sel otak dan membolehkan otak berfungsi secara normal.

Hasilnya, pesakit akan dapat pulih dari gejala psikotik dan melalui kehidupan yang normal semula.

Jenis-jenis Antipsikotik
1.

Antipsikotik Tipikal (juga dikenali sebagai antipsikotik generasi pertama):

o

Phenothiazines (Chlorpromazine, Thioridazine, Fluphenazine, Perphenazine, Prochlorperazine,

Trifluoperazine).

2.

Butyrophenones (Haloperidol)

Thioxanthenes (Flupenthixol, Zuclopenthixol)

Benzamides yang diubah (Sulpiride)

Antipsikotik Atipikal (juga dikenali sebagai antipsikotik generasi kedua):

o

Clozapine

Olanzapine

Risperidone

Quetiapine

Aripiprazole

Ziprasidone

Sertindole

Kesan Sampingan
Kesan sampingan yang dikaitkan dengan antipsikotik termasuklah :
1.

Kesan sampingan Ekstrapiramidal:

o

Kejang dan menggeletar (gejala Parkinson) biasa berlaku secara beransur-ansur pada pesakit
dewasa atau warga tua

Pergerakan muka dan badan yang tidak normal biasanya pada kanak-kanak atau remaja

Perasaan tidak selesa boleh berlaku selepas pengambilan dos yang tinggi

Pergerakan beritma tidak terkawal pada lidah, muka dan rahang biasanya berlaku selepas
rawatan jangka panjang atau dengan dos ubat yang tinggi

2.

Kesan sampingan yang lain

o

Peningkatan selera makan

Pertambahan berat badan

Perubahan paras gula dalam darah lalu meningkatkan risiko kencing manis

Kehilangan sel darah putih yang berfungsi melawan penyakit

Mengantuk

Tekanan darah rendah

Langkah Berjaga-jaga
Antipsikotik harus digunakan dengan berhati-hati dalam keadaan :

Kerosakan hati

Kerosakan ginjal

Masalah jantung

Penyakit Parkinson

Epilepsi (sawan)

Kemurungan

Myasthenia gravis (masalah fungsi otot disebabkan otot menjadi lemah)

Pembesaran prostat

Glaukoma

Peringatan

Jangan berhenti pengambilan ubat tanpa kebenaran doktor

Maklumat Am

Sebelum mengambil ubat ini, sila maklumkan kepada doktor tentang sejarah perubatan terutama tentang
penyakit hati atau ginjal serta alahan kepada ubat

Gabungan ubat ini dengan alkohol atau ubat-ubatan jenis sedatif yang lain boleh menyebabkan kesan
mengantuk yang kuat

Hadkan pengambilan alkohol

Guna dengan berhati-hati ke atas warga tua kerana mereka lebih terdedah kepada kesan sampingan ubat
ini

Penggunaan ubat ini semasa mengandung memerlukan perhatian rapi

Bincang tentang risiko dan kebaikan menggunakan ubat ini dengan doktor anda

Maklumkan kepada doktor anda jika anda menyusukan anak kerana dos ubat perlu diubah

Kaedah Penyimpanan

Kaedah penyimpanan perlu diberi lebih perhatian kerana ubat jenis ini selalu disalahguna

Jangan campurkan ubat ini dengan ubat-ubatan lain

Simpan ubat di dalam tempat yang sejuk, kering dan sukar dicapai oleh kanak-kanak

Antiepileptik (Sawan)
Pengenalan

Epilepsi merupakan sejenis penyakit yang disebabkan oleh perubahan cas elektrik yang tidak terkawal secara tibatiba pada bahagian otak dan mengganggu fungsi sistem saraf yang normal. Ini menyebabkan penghidapnya
mengalami sawan berulang kali atau tidak sedarkan diri dan tidak dapat mengawal pergerakan badan secara tibatiba. Kebiasaannya, epilepsi di rawat dengan menggunakan ubat antiepileptik atau ubat sawan.

Pemilihan ubat antiepileptik.

Terdapat pelbagai jenis ubat antiepileptik yang terdapat di Malaysia. Antaranya ialah carbamazepine, lamotrigine,
sodium valporate, levetiracetam, topiramate, phenytoin, gabapentine, clonazepam, dan phenobarbitone. Faktor
faktor yang akan dipertimbangkan untuk memulakan rawatan ubat antiepileptik adalah seperti berikut :
1.

Jenis epilepsi yang dialami

2.

Kemungkinan kesan sampingan

Antara kesan sampingan yang biasa dialami oleh pesakit yang mengambil ubat antiepileptik adalah seperti;
sakit kepala, pening, mengantuk, lemah badan, kurang kawalan otot, letih dan ketidakseimbangan
pergerakan.

3.

Kehamilan
Pesakit wanita adalah dinasihatkan untuk merancang kehamilan dengan baik agar risiko serangan sawan
kepada pesakit dan kesan sampingan ubat kepada bayi dalam kandungan dapat dielakkan. Pengambilan pil
kontraseptif ( pil perancang) bersama ubat antiepileptik boleh menyebabkan interaksi ubat berlaku yang
mana kemungkinan pil perancang menyebabkan paras ubat antiepileptik dalam darah berkurang seterusnya

akan meningkatkan risiko serangan sawan. Selain daripada itu, beberapa ubat antiepileptik juga boleh
mengurangkan kesan pil kontraseptif yang mungkin akan menyebabkan kehamilan yang tidak dirancang
seperti carbamazepine, lamotrigine, phenytoin dan topiramate.
4.

Interaksi ubat
Selain daripada interaksi ubat antiepileptic dengan pil kontraseptif, ada kemungkinan juga untuk berlaku
interaksi ubat di antara ubat antiepileptik yang lain sekiranya pesakit mengambil lebih daripada satu jenis
ubat antiepileptik, contohnya carbamazepine boleh mengurangkan paras sodium valproate dalam darah
yang boleh menyebabkan kemungkinan berlakunya serangan sawan. Oleh itu, doctor akan mencadangkan
pengambilan ubat pada dos yang bersesuaian sekiranya pesakit mengambil lebih daripada satu jenis
antiepileptik.

Dos ubat antiepileptik.

Doktor akan memberikan dos ubat antiepileptik yang bersesuaian kepada pesakit berdasarkan faktor faktor
pemilihan yang telah dibuat. Kebiasaannya, pesakit akan diberikan dos ubat yang rendah pada permulaan rawatan
dan akan ditingkatkan secara berperingkat sehingga dos pengekalan dicapai iaitu dos di mana ubat antiepileptik
tersebut dapat mengawal serangan sawan pesakit.

Perubahan ubat antiepileptik.

Sesetengah pesakit akan merasakan ubat antiepileptik yang diambil tidak lagi dapat mengawal serangan sawan
selepas satu tempoh tertentu. Ini mungkin berlaku akibat;

Pesakit tidak mengambil ubat secara konsisten

Tahap epilepsi pesakit telah berubah

Punca penyebab epilepsi pesakit telah berubah

Sistem saraf pesakit tidak lagi memberi maklumbalas kepada ubat antiepileptik tersebut

Apabila keadaan ini berlaku, pesakit haruslah segera berjumpa doktor untuk membuat perubahan kepada dos atau
jenis antiepileptik yang lebih bersesuaian.

Pemantauan paras ubat dalam darah.

Sesekali, ujian pemantauan paras ubat dalam darah akan dilakukan untuk memastikan pesakit mengambil ubat
dengan konsisten atau untuk mengenalpasti sekiranya kesan sampingan adalah disebabkan oleh dos ubat yang
terlalu tinggi. Selain daripada itu, pemantauan juga dibuat sekiranya pesakit ingin melakukan sebarang pembedahan
atau bagi pesakit wanita yang hamil.

Fakta penting yang perlu diberi perhatian.

Pengambilan ubat antiepileptik secara komplians iaitu dengan pengambilan ubat, dos dan masa yang betul, penting
bagi mengelakkan serangan sawan.
Laporkan kepada doktor sekiranya pesakit mengalami sebarang kesan sampingan ubat antiepileptik. alahan kepada
jenis ubat tertentu, mengambil ubat ubatan yang lain atau pil kontraseptif, mengandung atau sedang menyusukan
anak.

Berbincang dengan doktor sekiranya pesakit merancang atau sedang mengandung atau sedang menyusukan anak,
agar dos ubat antiepileptik dapat diubah mengikut kesesuaian pesakit. Jangan berhenti mengambil ubat antiepileptik
semasa mengandung kecuali atas arahan doktor.
Kadar serangan sawan mungkin berubah dari semasa ke semasa akibat perubahan tahap kesihatan yang mungkin
disebabkan oleh penuaan, tekanan atau menopaus seterusnya menyebabkan perubahan dos antiepileptik yang
diperlukan utnutk mengawal sawan.
Sesetengah ubat antiepileptik boleh menyebabkan kehilangan mineral dari tulang pesakit yang boleh meningkatkan
risiko osteoporosis dan patah tulang. Oleh itu, pesakit digalakkan untuk mengamalkan pemakanan dengan diet tinggi
kalsium dan vitamin D; elakkan merokok dan pengambilan alkohol.

Ubat Anti-Keresahan
Pengenalan

Ubat antikeresahan ialah ubat preskripsi menenangkan pesakit yang mengalami keresahan yang terlampau,
dan untuk merangsang tidur (sedatif atau alat bantu tidur).

Jenis ubat yang selalu digunakan ialah benzodiazepine.

Melegakan keresahan yang terlampau jika digunakan untuk tempoh yang singkat.

Ubat Preskripsi
Benzodiazepines
Ubat benzodiazepine yang sering digunakan untuk rawatan keresahan ialah:- Alprazolam (Xanax), Diazepam
(Valium) and Lorazepam (Ativan).
Penggunaan benzodiazepine adalah lebih selamat berbanding barbiturat memandangkan potensi penyalahgunaan,
kesan sampingan dan masalah interaksi benzodiazepine yang rendah. Kelebihan dos barbiturat adalah punca utama
kematian. Dos barbiturat yang berlebihan adalah punca utama kematian.

Jangkamasa tindakan
Benzodiazepine terbahagi kepada beberapa kumpulan bergantung kepada jangkamasa tindakan.
1.

Jangkamasa pendek
o

Bertindak kurang dari enam jam

Kesan ubat yang berpanjangan adalah sedikit sekiranya diambil sebelum tidur, tetapi kesukaran
tidur mungkin berulang dan menyebabkan keresahan di kala terjaga dari tidur.

2.

Berkesan untuk mengatasi masalah kesukaran untuk tidur

Jangkamasa sederhana
o

Bertindak selama 6-10 jam

Kesan ubat yang berpanjangan adalah sedikit

Kesukaran tidur yang berulang jarang berlaku

3.

Jangkamasa panjang (contohnya Lorazepam)

o

Kesan sedatif yang kuat dan berpanjangan

Pengumpulan ubat dalam badan boleh berlaku

Jangkamasa penyingkiran ubat berbeza di antara individu terutamanya warga emas

Lebih berkesan untuk membantu keresahan berbanding mengatasi masalah kesukaran tidur.

Alprazolam
Lebih berkesan sebagai anti-keresahan berbanding digunakan sebagai ubat tidur walaupun mempunyai jangka hayat
pendek.

Lorazepam
Berpotensi untuk memudaratkan lagi keadaan lupa dan keliru.
Bukan pilihan terbaik untuk kegunaan jangka panjang bagi warga emas disebabkan kesan pelupa
Mungkin pilihan terbaik untuk rawatan jangka pendek bagi pesakit muda yang tidak mengambil minuman beralkohol
memandangkan ubat ini kurang memberikan kesan sedatif.

Kesan sampingan

Mengantuk, koordinasi otot tidak seragam, kekeliruan, gayat, dan gangguan pertimbangan adalah kesan
sampingan yang biasa dialami.

Benzodiazepine mungkin mengganggu keupayaan untuk memandu dan mengendalikan jentera. Kesan
gangguan ini semakin buruk sekiranya diambil bersama dengan minuman beralkohol memandangkan keduaduanya bertindak pada sistem saraf pusat.

Pengambilan benzodiazepin bersama alkohol boleh menyebabkan kematian.

Kesan ubat benzodiazepine jangkamasa panjang juga boleh berpanjangan sehingga keesokan harinya.

Penggunaan benzodiazepine yang berpanjangan boleh menyebabkan masalah keresahan yang dialami
lebih teruk samada orang itu mempunyai sejarah psikiatrik atau tidak.

Kesan Mudarat
2 jenis kesan mudarat mungkin berlaku disebabkan penggunaan berpanjangan ubat anti keresahan:
1.

Kesan kebergantungan
o

Ubat ini boleh menyebabkan kesan kebergantungan sekiranya diambil secara berterusan selama 2
minggu.

2.

Kesan gian
o

Pemberhentian mendadak pengambilan ubat anti keresahan boleh mengakibatkan reaksi yang
teruk dan berpotensi mengancam nyawa, seperti juga kesan gian dari alkohol menyebabkan
kecelaruan.

Tempoh kesan gian di kalangan ubat berbeza-beza. Dalam tempoh 12 hingga 24 jam yang
pertama, seseorang itu mungkin berasa cemas, gelisah, terketar-ketar dan lemah.

Sawan mungkin terjadi pada mereka yang mengambil dos yang tinggi. Kadang-kadang, sawan
boleh berlaku 1 hingga 3 minggu selepas pemberhentian ubat.

Gejala gian benzodiazepine boleh berlaku bila-bila masa sehingga tempoh 3 minggu setelah

pemberhentian ubat jangkamasa panjang, tetapi boleh berlaku dalam tempoh beberapa jam sahaja
dengan ubat jangkamasa pendek.
Kesan-kesan lain yang boleh berlaku sewaktu pemberhentian ubat termasuklah penyahidratan,

kecelaruan, tidak boleh tidur, kekeliruan, dan halusinasi (melihat atau mendengar tentang benda yang
tiada disitu).

Langkah Berjaga-jaga
Jangan tingkatkan dos atau mengambil dos yang berlebihan daripada yang disarankan oleh doktor.
Walaupun kemungkinan kerosakan hati adalah kecil apabila ubat diambil pada dos yang telah disarankan, namun
masih perlu dipertimbangkan pada setiap individu, terutama mereka yang mengambil ubat-ubatan lain termasuklah
ubat penahan sakit dan/ atau alkohol

Arahan Khusus

Makan ubat bersama makanan atau susu sekiranya berlaku ketidakselesaan perut. Kesan toleransi ubat
kurang berkesan terjadi dengan penggunaan yang berpanjangan.

Jangan berhenti mengambil ubat ini tanpa kebenaran doktor.

Dos ubat anda mungkin perlu direndahkan sekiranya anda telah mengambilnya untuk satu tempoh yang
lama.

Maklumat Am

Sebelum mengambil ubat ini, sila beritahu doktor anda mengenai sejarah pengubatan terutamanya penyakit
hati atau ginjal, alahan ubat.

Alkohol atau jenis ubat sedatif lain akan mengakibatkan rasa amat mengantuk.

Hadkan pengambilan alkohol.

Warga emas adalah lebih sensitif terhadap kesan ubat ini. Guna dengan berhati-hati.

Ubat ini tidak disyorkan sewaktu hamil. Bincanglah dengan doktor anda mengenai risiko dan manfaat ubat
ini.

Ubat ini mungkin meresap ke dalam susu badan, sila rujuk doktor anda sebelum menyusukan anak anda.

Kaedah Penyimpanan

Memandangkan ubat ini sering disalahgunakan, kaedah penyimpanannya perlu diberi lebih perhatian.

Jangan campur ubat ini dengan ubat-ubatan lain.

Simpan ditempat yang sejuk, kering dan jauh dari kanak-kanak.

Ubat Anti-Kemurungan (Antidrepresi)

Pengenalan
Ubat antikemurungan (antidepresi) ialah ubat yang digunakan untuk melegakan tanda-tanda kemurungan. Ia juga
mempunyai kesan penenang. Terdapat empat jenis ubat anti kemurungan iaitu:

Trisiklik (Tricyclic)

RIMAs (Reversible Inhibitors of Monoamine Oxidase type A)

SSRIs (Selective Serotonin Reuptake Inhibitors)

SNRIs (Serotonin and Noradrenaline Reuptake Inhibitors)

Bagaimana ia bertindak?
Kemungkinan besar ubat ini menambah aktiviti bahan kimia di dalam otak yang dikenali sebagai pemancar neuro.
Pemancar neuro menghantar isyarat dari satu sel otak kepada sel otak yang lain. Bahan kimia yang terbabit dengan
kemurungan dikenali sebagai Serotonin dan Noradrenalin.

Bagaimana anda mengambil ubat ini?

Ambil ubat setiap hari seperti yang diarahkan. Jangan ubah dos ubat sendiri.

Kesan terapeutik ubat hanya boleh dilihat selepas dua minggu, jadi menunggu adalah penting.

Kesan sampingan ubat akan berkurangan setelah beberapa lama diambil.

Rujuk kepada doktor anda sekiranya kesan sampingan tidak disenangi. Doktor mungkin mencadangkan
ubat dari jenis yang lain.

Kesan Mudarat
Trisiklik
Kesan sampingan ubat trisiklik yang biasa adalah kering mulut, menggeletar, peningkatan degupan jantung,
sembelit, mengantuk dan kenaikan berat badan. Di kalangan warga emas, ubat ini mungkin menyebabkan
kekeliruan, kesukaran untuk membuang air kecil, rasa hendak pitam dan jatuh. Elak dari menggunakan trisiklik
sekiranya anda mempunyai masalah jantung. Bagi kaum lelaki, mereka mungkin mengalami mati pucuk atau
ejakulasi yang lambat.

RIMAs
Elakkan mengambil ubat RIMAs dengan makanan yang mengandungi Tyramine (contoh: keju, minuman beralkohol,
cokelat, dadih, sos soya) kerana ia boleh menyebabkan tekanan darah tinggi. Jika anda mengambil ubat RIMA,
doktor atau ahli farmasi akan memberikan anda senarai makanan yang perlu dielakkan.

SSRIs
Kesan sampingan pada perut adalah biasa dan ianya berkait rapat dengan dos ubat. Ini termasuklah rasa mual,
muntah, perut tidak selesa (dyspepsia), sakit perut, cirit birit, sembelit, tiada selera makan dan kehilangan berat
badan.
Terdapat
juga
kesan
sampingan
lain
yang
berkaitan
dengan
ubat
ini.
Sekiranya anda rasa kesan sampingan ini adalah disebabkan oleh SSRI yang anda ambil, sila sahkan dengan doktor
atau ahli farmasi.

SNRIs
Kesan sampingan ubat ini adalah serupa dengan SSRIs.

Langkah Berjaga-jaga

1. Memandu atau menggunakan jentera

Terdapat ubat antikemurungan yang menyebabkan kesan mengantuk dan melambatkan tindakbalas anda.
Sila rujuk kepada doktor anda sekiranya pekerjaan anda melibatkan pengendalian mesin atau pemanduan.

2. Gejala gian
Ubat antikemurungan selalunya tidak menyebabkan ketagihan tetapi sesetengah orang mungkin mengalami
gejala gian apabila mereka berhenti menggunakan ubat SSRIs or SNRIs. Kesannya termasuklah perut tidak
selesa, gejala selsema, keresahan, pening, mimpi ngeri pada waktu malam dan mengalami sensasi seperti
terkena kejutan elektrik. Bagi mengurangkan kesan sampingan ubat ini, doktor akan menurunkan dos ubat
secara berkala. Jangan berhenti mengambil ubat ini secara mendadak.

3. Golongan remaja
Jika mendapat preskripsi doktor, Ubat SSRIs boleh diambil oleh golongan yang berumur di bawah 18 tahun,
tetapi dengan lebih berhati-hati.

4. Kehamilan
Elakkan daripada menggunakan sebarang jenis ubat antikemurungan sewaktu hamil, terutamanya dalam
tempoh 3 bulan pertama kehamilan kerana ia menyebabkan risiko kecacatan pada bayi yang bakal
dilahirkan. Pada kebiasaannya rawatan alternatif akan dipertimbangkan kecuali dalam keadaan
kemurungan yang teruk dan boleh mengancam nyawa ibu atau anak, penggunaan ubat anti kemurungan
tidak dapat dielakkan.

Kaedah Penyimpanan
Simpan ubat anda di dalam bekas asal dan ditutup ketat. Simpan pada suhu bilik dan jauhkan daripada kanak-kanak,
keadaan panas dan kelembapan yang melampau.

A mood stabilizer is a psychiatric medication used to treat mood disorders characterized by intense
and sustained mood shifts, typicallybipolar disorder.
Contents
[hide]

1 Uses

2 Examples
o

2.1 Mineral

2.2 Anticonvulsants

2.3 Antipsychotics

2.4 Other

2.5 Combination therapy

3 Relationship to antidepressants

4 Mechanism

5 See also

6 References

Uses[edit]
Used to treat bipolar disorder,[1] mood stabilizers suppress swings between mania and depression.
Mood-stabilizing drugs are also used inborderline personality disorder[2] and schizoaffective disorder.

Examples[edit]
The term "mood stabilizer" does not describe a mechanism, but rather an effect. More precise
terminology is used to classify these agents.
Drugs commonly classed as mood stabilizers include:

Mineral[edit]

Lithium Lithium is the "classic" mood stabilizer, the first to be approved by the US FDA, and
still popular in treatment. Therapeutic drug monitoring is required to ensure lithium levels remain
in the therapeutic range: 0.6 or 0.8-1.2 mEq/L (or millimolar). Signs and symptoms of toxicity
include nausea, vomiting, diarrhea, and ataxia.[3] The most common side effects are lethargy and
weight gain. The less common side-effects of using lithium are blurred vision, slight tremble in
the hands, and a feeling of being mildly ill. In general, these side-effects occur in the first few
weeks after commencing lithium treatment. These symptoms can often be improved by lowering
the dose.[4]

Anticonvulsants[edit]
Many agents described as "mood stabilizers" are also categorized as anticonvulsants. The term
"anticonvulsant mood stabilizers" is sometimes used to describe these as a class. [5] Although this
group is also defined by effect rather than mechanism, there is at least a preliminary understanding
of the mechanism of most of the anticonvulsants used in the treatment of mood disorders. [citation needed]

Valproic acid (Depakine), divalproex sodium (Depakote), and sodium valproate (Depacon,
Epilim) Available in extended release form. This drug can be very irritating to the stomach,
especially when taken as valproic acid. Liver function and CBC should be monitored.[citation needed]

Lamotrigine (Lamictal) Particularly effective for bipolar depression. Usual dose is 100
200 mg daily, which can be built up by 25 mg every 2 weeks.[6] The patient should be monitored
for signs and symptoms of StevensJohnson syndrome, a very rare but potentially fatal skin
condition.[citation needed]

Carbamazepine (Tegretol) CBC should be monitored, as carbamazepine can lower white

blood cell count. Therapeutic drug monitoring is required. Carbamazepine was approved by
the US Food and Drug Administration as a bipolar disorder treatment in 2005, but had been
widely used previously.[citation needed]

Oxcarbazepine (Trileptal) Oxcarbazepine is not FDA approved for bipolar disorder. Still, it
appears to be effective in about one-half of patients with bipolar disorder and be well tolerated. [7]

There is insufficient evidence to support the use of various other anticonvulsants, such
as gabapentin and topiramate, as mood stabilizers.[8]

Antipsychotics[edit]

Some atypical
antipsychotics (aripiprazole, risperidone, olanzapine, quetiapine, asenapine, paliperidone, ziprasi
done, and lurasidone) also have mood stabilizing effects[9] and are thus commonly prescribed
even when psychotic symptoms are absent.[9]

Other[edit]

It is also conjectured that omega-3 fatty acids may have a mood stabilizing effect.
[10]

Compared with placebo, omega-3 fatty acids appear better able to augment known mood

stabilizers in reducing depressive (but perhaps not manic) symptoms of bipolar disorder;
additional trials would be needed to establish the effects of omega-3 fatty acids alone. [11]

It is known that even subclinical hypothyroidism can blunt a patient's response to both mood
stabilizers and antidepressants. Furthermore, preliminary research into the use of thyroid
augmentation in patients with refractory and rapid-cycling bipolar disorder has been positive,
showing a slowing in cycle frequency and reduction in symptoms. Most studies have been
conducted on an open-label basis. One large, controlled study of 0.300 mg daily dose of
levothyroxine (T4) found it superior to placebo for this purpose. The study, conducted in

Germany, has not been published in English. In general, studies have shown T4 to be welltolerated and to show efficacy even in patients without overt hypothyroidism.

Combination therapy[edit]
In routine practice, monotherapy is often not sufficiently effective for acute and/or maintenance
therapy and thus most patients are givencombination therapies.[12] Combination therapy (atypical
antipsychotic with lithium or valproate) shows better efficacy over monotherapy in the manic phase
in terms of efficacy and prevention of relapse.[12] However, side effects are more frequent and
discontinuation rates due to adverse events are higher with combination therapy than with
monotherapy.[12]

Relationship to antidepressants[edit]
Most mood stabilizers are primarily antimanic agents, meaning that they are effective at
treating mania and mood cycling and shifting, but are not effective at treating acute depression. The
principal exceptions to that rule, because they treat both manic and depressive symptoms,
are lamotrigine, lithium carbonate and quetiapine.
Nevertheless, antidepressants are still often prescribed in addition to mood stabilizers during
depressive phases. This brings some risks, however, as antidepressants can
induce mania, psychosis, and other disturbing problems in people with bipolar disorderin
particular, when taken alone. The risk of antidepressant-induced mania when given to patients
concomitantly on antimanic agents is not known for certain but may still exist. [13] The majority of
antidepressants appear ineffective in treating bipolar depression.[13]
Antidepressants cause several risks when given to bipolar patients. They are ineffective in treating
acute bipolar depression, preventing relapse, and can cause rapid cycling. Studies have been
shown that antidepressants have no benefit versus a placebo or other treatment. Antidepressants
can also lead to a higher rate of non-lethal suicidal behavior. Relapse can also be related to
treatment with antidepressants. This is less likely to occur if a mood stabilizer is combined with an
antidepressant, rather than an antidepressant being used alone. Evidence from previous studies
shows that rapid cycling is linked to use of antidepressants. Rapid cycling is defined as the presence
of four or more mood episodes within a year's time. Evidence suggests that rapid cycling and mixed
symptoms have become more common since antidepressant medication has come into widespread
use. There is a need for caution when treating bipolar patients with antidepressant medication due to
the risks that they pose.[citation needed]
Use of mood stabilizers and anticonvulsants such as lamotrigine, carbamazapine, valproate and
others may lead to chronic folate deficiency, potentiating depression.[citation needed] Also, "Folate

deficiency may increase the risk of depression and reduce the action of antidepressants." [14] Lmethylfolate (also formally known as 5-MTHF or Levofolinic acid), a centrally acting trimonoamine
modulator, boosts the synthesis of three CNS neurotransmitters: dopamine, norepinephrine and
serotonin. Mood stabilizers and anticonvulsants may interfere with folic acid absorption and Lmethylfolate formation. Augmentation with the medical food L-methylfolate may improve
antidepressant effects of these medicines, including lithium and antidepressants themselves, by
boosting the synthesis of antidepressant neurotransmitters.[citation needed] However, the U.S. National
Institutes of Health issued a warning caution about the use of L-methylfolate for patients with bipolar
disease. [1]

Mechanism[edit]
The precise mechanism of action of lithium is still unknown, and it is suspected that it acts at various
points of the neuron between the nucleus and the synapse. Lithium is known to inhibit the enzyme
GSK-3B. This has the effect relieving pressure on the circadian clock - which is thought to be often
malfunctioning in people with bipolar disorder - and positively modulates gene transcription of brainderived neurotrophic factor (BDNF). The resulting increase in neural plasticity may be central to
lithium's therapeutic effects. Lithium may also increase the synthesis of serotonin.
All of the anticonvulsants routinely used to treat bipolar disorder are blockers of voltage-gated
sodium channels, affecting the brain's glutamate system. For valproic acid, carbamazepine and
oxcarbazepine, however, their mood-stabilizing effects may be more related to effects on
the GABAergic system. Lamotrigine is known to decrease the patient's cortisol response to stress.
One possible downstream target of several mood stabilizers such as lithium, valproate, and
carbamazepine is the arachidonic acid cascade.[15]
An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in
the central and the peripheral nervous system. Anticholinergics inhibit parasympathetic nerve
impulses by selectively blocking the binding of the neurotransmitter acetylcholine to its receptor
in nerve cells. The nerve fibers of the parasympathetic system are responsible for the involuntary
movement of smooth muscles present in the gastrointestinal tract, urinary tract, lungs, etc.
Anticholinergics are divided into three categories in accordance with their specific targets in the
central and/or peripheral nervous system: antimuscarinic agents, ganglionic blockers,
and neuromuscular blockers.[1]
Contents
[hide]

1 Medical uses

2 Recreational uses

3 Side effects
o

3.1 Remedies

4 Pharmacology

5 Examples

6 Plant sources

7 Use as a deterrent

8 References

Medical uses[edit]
Anticholinergic drugs are used to treat a variety of conditions:

Gastrointestinal disorders (e.g., gastritis, diarrhea, pylorospasm, diverticulitis, ulcerative

colitis, nausea, and vomiting)

Genitourinary disorders (e.g., cystitis, urethritis, and prostatitis)

Respiratory disorders (e.g., asthma, chronic bronchitis, and chronic obstructive pulmonary
disease [COPD])

Sinus bradycardia due to a hypersensitive vagus nerve.

Insomnia, although usually only on a short-term basis.

Dizziness (including vertigo [a.k.a. 'the spins'] and motion sickness-related symptoms)

Anticholinergics generally have antisialagogue effects (decreasing saliva production), and most
produce some level of sedation, both being advantageous in surgical procedures. [2][3]

Recreational uses[edit]
When a significant amount of an anticholinergic is taken into the body, a toxic reaction known
as acute anticholinergic syndrome may result. This may happen accidentally or intentionally as a

consequence of recreational drug use. Anticholinergic drugs are usually considered the least
enjoyable by many recreational drug users,[4] possibly due to the lack of euphoria caused by them.
There have been reported cases of users experiencing what they attribute to "euphoria" from the use
of this substance. It also can produce extremely vivid hallucinations (visual, auditory, tactile) which
often can not be distinguished from reality; this can cause intense fear and panic and is more often
considered to be a poison rather than a recreational substance by those who have experimented
with this class of drug, and can result in death.[5] In terms of recreational use, these drugs are
commonly referred to as deliriants. Because most users do not enjoy the experience, they do not
use it again, or do so very rarely. The risk of addiction is low in the anticholinergic class. The effects
are usually more pronounced in the elderly, due to natural reduction of acetylcholine production
associated with age.

Side effects[edit]
Long term use increases the risk of both mental and physical decline.[6] It is unclear if they affect the
risk of death.[6] Possible effects of anticholinergics include:

Ataxia; loss of coordination

Dementia[7]

Decreased mucus production in the nose and throat; consequent dry, sore throat

Xerostomia or dry-mouth with possible acceleration of dental caries

Cessation of perspiration; consequent decreased epidermal thermal dissipation leading to

warm, blotchy, or red skin

Increased body temperature

Pupil dilation (mydriasis); consequent sensitivity to bright light (photophobia)

Loss of accommodation (loss of focusing ability, blurred vision cycloplegia)

Double-vision (diplopia)

Increased heart rate (tachycardia)

Tendency to be easily startled

Urinary retention

Diminished bowel movement, sometimes ileus (decreases motility via the vagus nerve)

Increased intraocular pressure; dangerous for people with narrow-angle glaucoma.

Possible effects in the central nervous system resemble those associated with delirium, and may
include:

Confusion

Disorientation

Agitation

Euphoria or dysphoria

Respiratory depression

Memory problems[8]

Inability to concentrate

Wandering thoughts; inability to sustain a train of thought

Incoherent speech

Irritability

Mental confusion (brain fog)

Wakeful myoclonic jerking

Unusual sensitivity to sudden sounds

Illogical thinking

Photophobia

Visual disturbances

Periodic flashes of light

Periodic changes in visual field

Visual snow

Restricted or "tunnel vision"

Visual, auditory, or other sensory hallucinations

Warping or waving of surfaces and edges

Textured surfaces

"Dancing" lines; "spiders", insects; form constants

Lifelike objects indistinguishable from reality

Phantom smoking

Hallucinated presence of people not actually there

Rarely: seizures, coma, and death

Orthostatic hypotension (sudden dropping of systolic blood pressure when standing up

suddenly) and significantly increased risk of falls in the elderly population. [9]

A common mnemonic for the main features of anticholinergic syndrome is the following:

Blind as a bat (dilated pupils)

Red as a beet (vasodilation/flushing)

Hot as a hare (hyperthermia)

Dry as a bone (dry skin)

Mad as a hatter (hallucinations/agitation)

Bloated as a Toad (ileus, urinary retention)

And the heart runs alone (tachycardia)

Remedies[edit]
Acute anticholinergic syndrome is completely reversible and subsides once all of the causative agent
has been excreted. Reversiblecholinergic agents such as physostigmine can be used in lifethreatening cases. Wider use is discouraged due to the significant side effects related to cholinergic
excess including: seizures, muscle weakness, bradycardia, bronchoconstriction, lacrimation,
salivation, bronchorrhea, vomiting, and diarrhea. Even in documented cases of anticholinergic
toxicity, seizures have been reported after the rapid administration of physostigmine. Asystole has
occurred after physostigmine administration for tricyclic antidepressant overdose, so a conduction
delay (QRS > 0.10 second) or suggestion of tricyclic antidepressant ingestion is generally
considered a contraindication to physostigmine administration.[10]
Piracetam (and other racetams), -GPC and choline are known to activate the cholinergic system
and alleviate cognitive symptoms caused by extended use of anticholinergic drugs. [citation needed]

Pharmacology[edit]
Anticholinergics are classified according to the receptors that are affected:

Antimuscarinic agents operate on the muscarinic acetylcholine receptors. The majority of

anticholinergic drugs are antimuscarinics.

Antinicotinic agents operate on the nicotinic acetylcholine receptors. The majority of these
are non-depolarising skeletal muscle relaxants for surgical use that are structurally related
to curare. Several are depolarizing agents.

Examples[edit]
Examples of common anticholinergics:

Anti-Muscarinic agents

Atropine

Benztropine (Cogentin)

Biperiden

Chlorpheniramine (Chlor-Trimeton)

Dicyclomine (Dicycloverine)

Dimenhydrinate (Dramamine)

Diphenhydramine (Benadryl, Sominex, Advil PM, etc.)

Doxylamine (Unisom)

Glycopyrrolate (Robinul)

Hydroxyzine (Atarax, Vistaril)

Ipratropium (Atrovent)

Orphenadrine

Oxitropium (Oxivent)

Oxybutynin (Ditropan, Driptane, Lyrinel XL)

Tolterodine (Detrol, Detrusitol)

Tiotropium (Spiriva)

Trihexyphenidyl

Scopolamine

Solifenacin

Tropicamide[4]

Anti-Nicotinic agents

Bupropion (Zyban, Wellbutrin) - Ganglion blocker[citation needed]

Dextromethorphan - Cough suppressant and ganglion blocker[citation needed]

Doxacurium - Nondeplorizing skeletal muscular relaxant

Hexamethonium - Ganglion blocker

Mecamylamine - Ganglion blocker and occasional smoking cessation aid[11]

Tubocurarine - Nondepolarizing skeletal muscular relaxant

Plants of the Solanaceae family contain various anticholinergic tropane alkaloids, such
as scopolamine, atropine, and hyoscyamine.

Physostigmine is one of only a few drugs that can be used as an antidote for anticholinergic
poisoning. Nicotine also counteracts anticholinergics by activating nicotinic acetylcholine
receptors. Caffeine (although an adenosine receptor antagonist) is able to counteract the
anticholinergic symptoms by reducing sedation and increasing acetylcholine activity, thereby causing
alertness and arousal.

Plant sources[edit]
The most common plants containing anticholinergic alkaloids are:

Atropa belladonna (Deadly Nightshade), source of atropine

Brugmansia species (Brugmansia)

Datura species (Datura)

Hyoscyamus niger (Henbane)

Mandragora officinarum (Mandrake)

Use as a deterrent[edit]
Certain preparations of some drugs with abuse potential, such as hydrocodone, are mixed with an
anticholinergic agent to deter intentional overdose. [12] Examples
include Hydromet/Hycodan (hydrocodone/homatropine) and Lomotil (diphenoxylate/atropine).[13]

Pseudoparkinsonism
(Parkinsonism)
Parkinsonism refers to any condition that causes Parkinson's-type
abnormal movements. These movements are caused by changes in or
destruction of the nerve cells in the area of the brain that controls
muscle movement, and results in a resting tremor, stiff muscles, slow
movements, and difficulty maintaining balance and walking. Certain drugs

and toxins that interfere with control of muscle movement can produce a
disorder called drug-induced Parkinsonism (DIP).
Drug-induced Parkinsonism is often reversible, especially if the offending
drug is discontinued early; however DIP may persist after drug
withdrawal. been described with a great diversity of compounds such as
antiemetics, drugs used for the treatment of vertigo, antidepressants,
calcium channel antagonists, antiarrythmics, antiepileptics,
cholinomimetics and other drugs.
Pseudoparkinsonism, or neuroleptic-induced parkinsonism, is aspecific type
of drug-induced Parkinson's and includes slow pill-rolling finger tremors,
masklike facial expression, weakened voice, absence of arm swing and
flexion of the arms at near 90% when walking, stiff stooped posture, and
an impaired shuffling gait. Cogwheeling rigidity, a ratchet-like motion of
the extremities during extension, is also seen.. Mentally, the client can
display a slowed ability to think through familiar situations
(bradyphrenia).
If you believe you have Parkinsonism due to use of a medication, then you
should see the physician who prescribed the medication or see a Family
Practice, Internal Medicine, or Neurology specialist.

Akathisia
From Wikipedia, the free encyclopedia

Akathisia
Classification and external resources

ICD-10

G21.1

ICD-9

781.0, 333.99

DiseasesDB

32479

eMedicine

neuro/362 emerg/338

MeSH

D011595

Typical symptoms of akathisia (note that the patient is forced to eat while standing instead of sitting).

Akathisia, or acathisia (from Greek kathzein "to sit", a- indicating negation or absence,
lit. "inability to sit") is a movement disorder characterized by a feeling of inner restlessness and a
compelling need to be in constant motion, as well as by actions such as rocking while standing or
sitting, lifting the feet as if marching on the spot, and crossing and uncrossing the legs while sitting.
People with akathisia are unable to sit or keep still, complain of restlessness, fidget, rock from foot to
foot, and pace.[1]
The term was coined by the Czech neuropsychiatrist Ladislav Haskovec (18661944), who
described the phenomenon in 1901.[2][3]
Antipsychotics (also known as neuroleptics), particularly the first generation antipsychotics, may
cause akathisia. Other known causes include side effects of certain medications, and nearly
any physically addictive drug during drug withdrawal.[4] It is also associated with Parkinson's
disease and related syndromes.[5]
Contents
[hide]

1 Description

2 Epidemiology

3 Diagnosis
o

3.1 Classification
4 Causes

4.1 Pathophysiological

4.2 Drug-Induced

5 Treatment

6 References

Description[edit]
Akathisia may range in intensity from a sense of disquiet or anxiety, to excruciating discomfort,
particularly in the knees. Patients typically pace for hours because the pressure on the knees
reduces the discomfort somewhat; once their knees and legs become fatigued and they are unable
to continue pacing, they sit or lie down, although this does not relieve the akathisia. At high doses or
with potent drugs such as haloperidol (Haldol) or chlorpromazine (Thorazine/Largactil), the feeling
can last all day from awakening to sleep. The anticholinergic medication procyclidine reduces
neuroleptic-induced akathisia to a certain degree, in addition to preventing and sometimes
eliminating the muscle stiffness that can occur alongside akathisia. When misdiagnosis occurs in
antipsychotic neuroleptic-induced akathisia, more antipsychotic neuroleptics may be prescribed,
potentially worsening the symptoms.[5] High-functioning patients have described the feeling as a
sense of inner tension and torment or chemical torture. Many patients describe symptoms
of neuropathic pain akin to fibromyalgia and restless legs syndrome.[6] In Han et al. (2013), the
authors describe restless legs syndrome's relation to akathisia, "Some researchers regard RLS as a
'focal akathisia' [in the legs]."[7] Although these side effects disappear quickly and remarkably when
the medication is stopped, tardive, or late-persisting akathisia may go on long after the offending
drug is discontinued, sometimes for a period of yearsunlike the related tardive dyskinesia, which
can be permanent.
Healy, et al. (2006), described the following regarding akathisia: tension, insomnia, a sense of
discomfort, motor restlessness, and marked anxiety and panic. Increased labile affect can result,
such as weepiness. Interestingly, in some people, the opposite response to SSRIs occurs, in the
form of emotional blunting, but sufficient clinical research has not yet been made in this area. [8]
Severe akathisia can become a very harrowing experience. Jack Henry Abbot (1981) describes the
sensation:[9]
...[It comes] from so deep inside you, you cannot locate the source of the pain The muscles of
your jawbone go berserk, so that you bite the inside of your mouth and your jaw locks and the pain
throbs. Your spinal column stiffens so that you can hardly move your head or your neck and
sometimes your back bends like a bow and you cannot stand up. You ache with restlessness, so
you feel you have to walk, to pace. And then as soon as you start pacing, the opposite occurs to you;
you must sit and rest. Back and forth, up and down you go you cannot get relief
In a psychiatric setting, patients who suffer from neuroleptic-induced akathisia often react by refusing
treatment.[10]

Epidemiology[edit]

Published epidemiological data for akathisia are mostly limited to treatment periods preceding the
arrival of second-generation antipsychotics.[11] Sachdev (1995)[12] reported an incidence rate of acute
akathisia of 31% for 100 patients treated for 2 weeks with antipsychotic medications. Sachdev
(1995) reported a prevalence range from 0.1% to 41%. [12]In all likelihood, rates of prevalence are
lower for current treatment as second-generation antipsychotics carry a lower risk of akathisia. [11]

Diagnosis[edit]
The presence and severity of akathisia can be measured using the Barnes Akathisia Scale,[13]
[14]
which assesses both objective and subjective criteria. [13] Precise assessment of akathisia is
problematic, as it is difficult to differentiate from a multitude of disorders with similar symptoms. In a
study of movement disorders induced by neuroleptics, akathisia was found in only 26% of patients
originally diagnosed with akathisia.[10] The primary distinguishing features of akathisia in comparison
with other syndromes are primarily subjective characteristics, such as the feeling of inner
restlessness.[15] Akathisia can commonly be mistaken for agitation secondary to psychotic symptoms
or mood disorder, antipsychotic dysphoria, restless legs syndrome (RLS), anxiety, insomnia, drug
withdrawal states, tardive dyskinesia, or other neurological and medical conditions.[16]
Additionally, the controversial diagnosis of "pseudoakathisia" is given, as noted by Mark J. Garcia. In
his article discussing akathisia among adults with severe and profound intellectual disability, he
describes pseudoakathisia as "comprising all the symptoms of abnormal movements seen with
akathisia, but without a sense of restlessness".[17]

Classification[edit]
Acute akathisia[16]

Pseudoakathisia[16]

Duration of less than 6 months

Motor manifesta

Develops soon after:

Predominantly in

starting antipsychotic medication or following dose increase

Possibly late sta

switching to a high-potency antipsychotic

No dysphoria

withdrawal of an anticholinergic medication

No awareness o

Motor fidgetines

Intense dysphoria

Awareness of restlessness

Great overlap w
Tardive akathisia[16]

Complex and semipurposeful motor fidgetiness

Chronic akathisia[16]

Delayed onset (

Not related to a

Persists for over 6 months after last dosage increment

Subjective sense of restlessness may be less marked

Mild dysphoria

Awareness of restlessness

Motor fidgetiness with stereotyped movement

Limb and orofacial dyskinesia often present

Significantly ass
Withdrawal or "rebo

Associated with

Onset usually w

Anticholinergic d

Causes[edit]
Pathophysiological[edit]
Han et al. (2013)[7] reported that upon examination of three patients who experienced abrupt onset
of restlessness characteristic of akathisia and RLS, magnetic resonance imaging of
the brain revealed pontine infarction (lack of blood to the pons area of the brain). Han et al. wrote,
"The features of our three patients suggest that RLS and akathisia may have a common
pathophysiological mechanism related to the pontine region of the brain." [7]

Drug-Induced[edit]
Akathisia is frequently associated with the use of dopamine receptor antagonist antipsychotic drugs.
[16]
Understanding is still limited on the pathophysiology of akathisia, but it is seen to be associated
with medications which block dopaminergic transmission in the brain. Additionally, drugs with
successful therapeutic effects in the treatment of medication-induced akathisia have provided
additional insight into the involvement of other transmitter systems. These
include benzodiazepines, -adrenergic blockers, and serotonin antagonists.[16] Another major cause
of the syndrome is the withdrawal of various addictive drugs in dependent individuals.[4]
It has been correlated with Parkinson's disease and related syndromes.[5] It is unclear, however,
whether this is due more to Parkinson's or the drugs used to treat it, such
ascarbidopa/levodopa (levocarb).[18]
Antidepressants can also induce the appearance of akathisia.[19][20][21][22] The 2006 UK study by Healy et
al. observed that akathisia is often miscoded in antidepressant clinical trials as "agitation, emotional
lability, and hyperkinesis (overactivity)".[8] The study further points out that misdiagnosis of akathisia
as simple motor restlessness occurs, but that this is more properly classed as dyskinesia. Moreover,
it shows links between antidepressant-induced akathisia and violence, including suicide, since
akathisia can "exacerbatepsychopathology", going on to state extensive clinical evidence correlates
akathisia with SSRI useabout ten times as many patients on SSRIs compared to placebo (5.0%
versus 0.5%) showed symptoms severe enough to drop out of a trial. [8]

It was discovered that akathisia involves increased levels of the neurotransmitter norepinephrine,
which is associated with mechanisms that regulate aggression, alertness, andarousal.[23] Though no
further research has been done yet, it may also be involved with disrupted NMDA channels in the
brain, which have both synergistic and regulatory effects on norepinephrine.
A single study observed that methylphenidate (Ritalin) appeared to cause akathisia in a single
patient.[24]
The table below summarizes factors that can induce akathisia, grouped by type, with examples or
brief explanations for each:

Catego
ry

Examples

Haloperidol (Haldol), droperidol, pimozide, trifluoperazine, amisulpride, risperi

Antipsyc
done, aripiprazole (Abilify), lurasidone (Latuda), ziprasidone(Geodon),
hotics[25]
andasenapine (Saphris)

SSRIs[26]

Fluoxetine (Prozac),[26] paroxetine (Paxil),[8] citalopram (Celexa)

Antidepr
Venlafaxine (Effexor), tricyclics, and trazodone (Desyrel)
essants

Antieme
Metoclopramide (Reglan), prochlorperazine (Compazine), and promethazine
tics

Antihist
amines

Cyproheptadine (Periactin) or diphenhydramine (Benadryl) this is more

commonly seen at very high doses

Drug
withdra
wal

Opioid withdrawal, barbiturates withdrawal, cocaine withdrawal

Serotoni
n
Harmful combinations of psychotropic drugs
syndrom
e

Treatment[edit]
Akathisia is sometimes reversible once the causative agent has been identified and discontinued,
but in some cases may become permanent.[27] Case reports and small randomized studies
suggest benzodiazepines, propranolol, and anticholinergics may help treat acute akathisia, but are
much less effective in treating chronic akathisia.[11] Taylor et al. found success in lowering the dose of
antipsychotic medication as an initial response to drug-induced akathisia, [17] which should be done
gradually, if possible.[11] To minimize the risk of akathisia from antipsychotics, the clinician is advised
to be conservative when increasing dosages.[17]
If the patient is experiencing akathisia due to opioid withdrawal, and continuing use of opioids is not
viable, drugs typically prescribed for acute idiopathic akathisia can be effective. GABA
analogues pregabalin and gabapentin, as well as drugs approved for treating RLS, may also be
effective in certain cases.[citation needed]
One study showed vitamin B6 to be effective for the treatment of neuroleptic-induced akathisia.[28]
N-acetyl cysteine also showed a positive effect on akathisia in a randomized control trial.[29]
Additional pharmacologic interventions found to have antiakathisia effects (especially for neurolepticinduced akathisia) include -adrenergic antagonists (e.g., propranolol), benzodiazepines
(e.g., lorazepam), anticholinergics (e.g., benztropine), and serotonin
antagonists (e.g., cyproheptadine) as an alternative.[16]
Trihexyphenidyl has also been prescribed to treat akathisia.

Dyskinesia
From Wikipedia, the free encyclopedia

Not to be confused with Dyskinetic cerebral palsy.

[hide]This article has multiple issues. Please help improve it or discuss the

This article provides insufficient context for those unfamiliar with the su
This article may be too technical for most readers to understand.

(Novembe

This article may be confusing or unclear to readers. In particular, it assume

No suggestions on talk.

Dyskinesia

(November 2013)

Classification and external resources

ICD-10

G24.9

ICD-9

333.8

DiseasesDB

17912

Patient UK

Dyskinesia

MeSH

D020820

Dyskinesia refers to a category of movement disorders that are characterized by involuntary muscle
movements,[1] including movements similar to tics or chorea and diminished voluntary movements.
[2]

Dyskinesia can be anything from a slight tremor of the hands to an uncontrollable movement of the

upper body or lower extremities. Discoordination can also occur internally especially with the
respiratory muscles and it often goes unrecognized. [3] Dyskinesia is a symptom of several medical
disorders that are distinguished by their underlying cause.
Contents
[hide]

1 Types
o

1.1 Medication-induced dyskinesias

1.2 Chronic/tardive

1.3 Non-motor

2 See also

3 References

4 Works cited

Types[edit]
This section may

requirecleanup to meet
Wikipedia'squality standards.
The specific problem is: title
does not match body. (August
2011)

Medication-induced dyskinesias[edit]
Acute dystonia is a sustained muscle contraction that sometimes appears soon after administration
of antipsychotic medications.[4] Any muscle in the body may be affected, including the jaw, tongue,
throat, arms, or legs. When the throat muscles are involved, this type of dystonia is called an
acute laryngospasm and is a medical emergency because it can impair breathing.[4] Older
antipsychotics such as Haloperidol or Fluphenazine are more likely to cause acute dystonia than
newer agents. Giving high doses of antipsychotics by injection also increases the risk of developing
acute dystonia.[4]
Levodopa-induced dyskinesia (LID) is evident in patients with Parkinson's disease who have been
on levodopa (L-DOPA) for prolonged periods of time. LID commonly first appears in the foot, on the
most affected side of the body. There are three main types that can be classified on the basis of their
course and clinical presentation following an oral dose of L-DOPA:[5][6]

Off-period dystonia correlated to the akinesia that occurs before the full effect of L-DOPA
sets in, when the plasma levels of L-DOPA are low. In general, it occurs as painful spasms in the
foot. Patients respond to L-DOPA therapy.[5][6]

Diphasic dyskinesia occurs when plasma L-DOPA levels are rising or falling. This form
occurs primarily in the lower limbs (though they can happen elsewhere) and is
usually dystonic (characterized by apparent rigidity within muscles or groups thereof)
or ballistic (characterized by involuntary movement of muscles) and will not respond to L-DOPA
dosage reductions.[5][6]

Peak-dose dyskinesia the most common form of levodopa-induced dyskinesia; it

correlates with the plateau L-DOPA plasma level. This type usually involves the upper limbs
more (but could also affect the head, trunk and respiratory muscles), is choreic (of chorea), and
less disabling. Patients will respond to L-DOPA reduction but may be accompanied by
deterioration of parkinsonism.[5][6] Peak-dose L-DOPA-induced dyskinesia has recently been
suggested to be associated with cortical dysregulation of dopamine signaling. [7]

Chronic/tardive[edit]
Late-onset dyskinesia, also known as tardive dyskinesia, occurs after long-term treatment with
an antipsychotic drug such as haloperidol (Haldol) or amoxapine (Asendin). The symptoms include
tremors and writhing movements of the body and limbs, and abnormal movements in the face,
mouth, and tongue including involuntary lip smacking, repetitive pouting of the lips, and tongue
protrusions.[8]
Rabbit syndrome is another type of chronic dyskinesia, while orofacial dyskinesia may be related to
persistent replication of Herpes simplex virus type 1.[9]

Non-motor[edit]
Two other types primary ciliary dyskinesia and biliary dyskinesia are caused by specific kinds of
ineffective movement of the body, and are not movement disorders.
Spastic thrusting of hip area can occur in sodemytopic Parkinson's.[jargon]

See also[edit]

Extrapyramidal symptoms
From Wikipedia, the free encyclopedia

This article needs additional citations for verification. Please

help improve this article by adding citations to reliable sources. Unsourced
material may be challenged and removed. (July 2013)

Extrapyramidal symptoms
Classification and external resources

ICD-9

333.90

Extrapyramidal symptoms (EPS), also known as extrapyramidal side effects (EPSE), are drug
induced movement disorders that include acute and tardive symptoms. These symptoms
include dystonia (continuous spasms and muscle contractions), akathisia(motor
restlessness), parkinsonism (characteristic symptoms such as rigidity, bradykinesia, and tremor),
and tardive dyskinesia(irregular, jerky movements). [1] Antipsychotics are often discontinued due to
inefficacy or intolerable side effects such as extrapyramidal symptoms. [2]

Since it is difficult to measure extrapyramidal symptoms, rating scales are commonly used to assess
the severity of movement disorders. The Simpson-Angus Scale (SAS), Barnes Akathisia Rating
Scale (BARS), Abnormal Involuntary Movement Scale (AIMS), and Extrapyramidal Symptom Rating
Scale (ESRS) are rating scales frequently used for such assessment and are not weighted for
diagnostic purposes. [1]
Contents
[hide]

1 Causes

2 Conditions

3 Treatment

4 See also

5 References

Causes[edit]
Extrapyramidal symptoms are most commonly caused by typical antipsychotic drugs that antagonize
dopamine D2 receptors. [1] The most common typical antipsychoticsassociated with EPS
are haloperidol and fluphenazine. [3] Atypical antipsychotics have lower D2 receptor affinity or higher
serotonin 5-HT2A receptor affinity which lead to lower rates of EPS. [4] However, some research has
shown that atypical antipsychotics are just as likely as conventional antipsychotics to cause EPS. [1]
Other anti-dopaminergic drugs like the antiemetic, metoclopramide, can also result in extrapyramidal
side effects. [5] Short and long-term use of antidepressants such as selective serotonin reuptake
inhibitors (SSRI), serotonin-norepinephrine reuptake inhibitors (SNRI), and norepinephrinedopamine reuptake inhibitors (NDRI) have also resulted in
EPS. [6]Specifically, duloxetine, sertraline, escitalopram, fluoxetine, and bupropion have been linked
to the induction of EPS. [6] Other causes of extrapyramidal symptoms can include brain damage and
meningitis. [7] [8]

Conditions[edit]

Acute dystonic reactions: muscular spasms of neck, jaw, back, extremities, eyes, throat, and
tongue; highest risk in young men [1]

Akathisia: A feeling of internal motor restlessness that can present as tension, nervousness,
or anxiety [1]

Pseudoparkinsonism: drug-induced parkinsonism (rigidity, bradykinesia, tremor, masked

facies, shuffling gait, stooped posture, sialorrhoea, and seborrhoea; greater risk in the

elderly). [1] Although Parkinson's disease is primarily a disease of the nigrostriatal pathway and
not the extrapyramidal system, loss of dopaminergic neurons in thesubstantia nigra leads to
dysregulation of the extrapyramidal system. Since this system regulates posture and skeletal
muscle tone, a result is the characteristic bradykinesiaof Parkinson's.

Tardive dyskinesia: involuntary muscle movements in the lower face and distal extremities;
this is a chronic condition associated with long term use of antipsychotics. [1]

Treatment[edit]
Anticholinergic drugs are used to control neuroleptic-induced EPS, although akathisia may
require beta blockers or even benzodiazepines. If the EPS are induced by anantipsychotic, EPS may
be reduced by dose titration or by switching to an atypical antipsychotic, such
as aripiprazole, ziprasidone, quetiapine, olanzapine, risperidone, orclozapine. These medications
possess an additional mode of action that is believed to negate their effect on
the nigrostriatal pathway, which means they are associated with fewer extrapyramidal side-effects
than "conventional" antipsychotics (chlorpromazine, haloperidol, etc.), Although some research has
shown that second generation neuroleptics cause EPS at the same rate as the first generation
drugs. [1]
Commonly used medications for EPS are anticholinergic agents such
as benztropine (Cogentin), diphenhydramine (Benadryl), and trihexyphenidyl (Artane). Another
common course of treatment includes dopamine agonist agents such as pramipexole. These
medications reverse the symptoms of extrapyramidal side effects caused by antipsychotics or other
drugs that either directly or indirectly inhibit dopaminergic neurotransmission.
Studies are yet to be undertaken on the optimum dosage of the causative drugs to reduce their side
effects (extrapyramidal symptoms (EPS)).

Dystonia
From Wikipedia, the free encyclopedia

Dystonias

A person with medication-induced dystonia.

Classification and external resources

ICD- G24.9
10

ICD- 333
9

OMI

128100 224500314250 128101128230 602629602124 11

8800601042 128200159900 128235607671 6074886120

67 612406612126 611031 611147

Dise 17912
ases
DB

NCI

Dystonia

MeS D004421
H

Gen
eRev

Dystonia Overview
Early-Onset Primary Dystonia (DYT1)

iews

Dystonia is a neurological movement disorder, in which sustained muscle contractions cause

twisting and repetitive movements or abnormal postures.[1] The movements may resemble a tremor.
Dystonia is often initiated or worsened by voluntary movements, and symptoms may overflow into
adjacent muscles.[2]
The disorder may be hereditary or caused by other factors such as birth-related or other physical
trauma, infection, poisoning (e.g.,lead poisoning) or reaction to pharmaceutical drugs,
particularly neuroleptics.[1] Treatment must be highly customized to the needs of the individual and
may include oral medications, botulinum neurotoxin injections, physical therapy and/or other
supportive therapies, and/or surgical procedures such as deep brain stimulation.
Contents
[hide]

1 History

2 Classification
o

2.1 Types of dystonia

2.2 Generalized dystonias

2.3 Focal dystonias

2.4 Segmental dystonias

2.5 Genetic / primary

3 Signs and symptoms

4 Causes

5 Treatment

5.1 Physical intervention

5.2 Medication

5.3 Surgery
6 See also

7 References

8 External links

History[edit]
The term "dystonia" was first used in 1911, by Hermann Oppenheim.[3]

Classification[edit]
There are multiple types of dystonia, and numerous diseases and conditions may cause dystonia.
Dystonia is classified by: 1. Clinical characteristics such as age of onset, body distribution, nature of
the symptoms, and associated features such as additional movement disorders or neurological
symptoms, and 2. Cause (which includes changes or damage to the nervous system and
inheritance).[2] Physicians use these classifications to guide diagnosis and treatment.

Types of dystonia[edit]

Generalized

Focal

Segmental

Psychogenic

Acute Dystonic Reaction[4]

Vegetative-vascular

Generalized dystonias[edit]

Normal birth history and milestones

Autosomal dominant

Childhood onset

Starts in lower limbs and spreads upwards

Also known as torsion dystonia or idiopathic torsion dystonia (old terminology "dystonia
musculorum deformans")

Focal dystonias[edit]
Main article: Focal dystonia
These are the most common dystonias and tend to be classified as follows:

Name

Anismus

Location

muscles of

Causes painful defecation, constipation; may be

the rectum

complicated by encopresis.

Cervical dystonia

muscles of

(spasmodic torticollis)

the neck

muscles
Blepharospasm

Description

around
theeyes

Causes the head to rotate to one side, to pull down

towards the chest, or back, or a combination of these
postures.

The sufferer experiences rapid blinking of the eyes or even

their forced closure causing functional blindness.

An extreme and sustained (usually) upward deviation of the

eyes often with convergence causing diplopia(double
Oculogyric crisis

muscles of

vision). It is frequently associated with backward and lateral

eyes and

flexion of the neck and either widely opened mouth or jaw

head

clenching. Frequently a result of antiemeticssuch as

the neuroleptics (e.g., prochlorperazine)
or metoclopramide. Also can be caused by Chlorpromazine

muscles of
Oromandibular

the jaw

dystonia

andmuscles
of tongue

Causes distortions of the mouth and tongue.

Spasmodic
dysphonia/Laryngeal
dystonia

muscles of

Causes the voice to sound broken, become hoarse,

larynx

sometimes reducing it to a whisper.

It interferes with activities such as writing or playing a

musical instrument by causing involuntary muscular
Focal hand dystonia

single muscle

(also known as

or small group

musician's or writer's

of muscles in

cramp).

the hand

contractions. The condition is sometimes "task-specific,"

meaning that it is generally apparent during only certain
activities. Focal hand dystonia is neurological in origin, and
is not due to normal fatigue. The loss of precise muscle
control and continuous unintentional movement results in
painful cramping and abnormal positioning that makes
continued use of the affected body parts impossible.

The combination of blepharospasmodic contractions and oromandibular dystonia is called cranial

dystonia or Meige's syndrome.

Segmental dystonias[edit]
Segmental dystonias affect two adjoining parts of the body:

Hemidystonia affects an arm and foot on one side of the body.

Multifocal dystonia affects many different parts of the body.

Generalized dystonia affects most of the body, frequently involving the legs and back.

Genetic / primary[edit]
Symbo
l

OMIM

Gene

Locus

Alt Name

DYT1

128100 TOR1A

9q34

Early-onset torsion dystonia

DYT2

224500 unknown

unknown

Autosomal recessive torsion dystonia

DYT3

314250 TAF1

Xq13

X-linked dystonia-parkinsonism

DYT4

128101 TUBB4[5]

19p13.12-13

Autosomal dominant whispering dysphonia

DYT5a 128230 GCH1

14q22.1-q22.2

DYT5b 191290 TH[disambiguation needed]

11p15.5

DYT6

602629 THAP1

8p11.21

DYT7

602124 unknown

DYT8

DYT9

Autosomal dominant dopamine-responsive

dystonia

Autosomal recessive dopamine-responsive

dystonia

Autosomal dominant dystonia with craniocervical predilection

18p

Autosomal dominant primary focal cervical

(questionable)

dystonia

118800 MR1

2q35

Paroxysmal nonkinesigenic dyskinesia

601042 SLC2A1

1p35-p31.3

Episodic choreoathetosis/spasticity (now

known to be synonymous with DYT18)

DYT10 128200 PRRT2

16p11.2-q12.1

Paroxysmal kinesigenic dyskinesia

DYT11 159900 SGCE

7q21

Myoclonic dystonia

DYT12 128235 ATP1A3

19q12-q13.2

DYT13 607671 unknown, near

1p36.32-

Rapid onset dystonia parkinsonism and

alternating hemiplegia of childhood

Autosomal dominant cranio-cervical/upper

D1S2667[6]

DYT14

p36.13

limb dystonia in one Italian family

See
DYT5

DYT15 607488 unknown

18p11[7]

DYT16 612067 PRKRA

2q31.3

DYT17 612406

unknown, near

20p11.2-

D20S107

q13.12

[8]

Myoclonic dystonia not linked to SGCE

mutations

Autosomal recessive young onset dystonia

parkinsonism

Autosomal recessive dystonia in one family

DYT18 612126 SLC2A1

1p35-p31.3

Paroxysmal exercise-induced dyskinesia

DYT19 611031 probably PRRT2

16q13-q22.1

DYT20 611147 unknown

2q31

Paroxysmal nonkinesigenic dyskinesia 2

DYT21 614588 unknown

2q14.3-q21.3

Late-onset torsion dystonia

DYT24 610110 ANO3[9]

11p14.2

Episodic kinesigenic dyskinesia 2, probably

synonymous with DYT10

Autosomal dominant cranio-cervical

dystonia with prominent tremor

There is a group called myoclonus dystonia or myoclonic dystonia, where some cases are hereditary
and have been associated with a missense mutation in the dopamine-D2 receptor. Some of these
cases have responded remarkably to alcohol.[10][11]

Other genes that have been associated with dystonia include CIZ1, GNAL, ATP1A3 and PRRT2.
[12]

Another report has linked THAP1 and SLC20A2 to dystonia.[13]

Signs and symptoms[edit]

Hyperglycemia-induced involuntary movements, which, in this case, did not consist of typical hemiballismus but
rather of hemichorea (dance-like movements of one side of the body;initial movements of the right arm in the
video) and bilateral dystonia (slow muscle contraction in legs, chest, and right arm) in a 62-year-old Japanese
woman with type 1 diabetes.

Symptoms vary according to the kind of dystonia involved. In most cases, dystonia tends to lead to
abnormal posturing, in particular on movement. Many sufferers have continuous pain, cramping, and
relentless muscle spasms due to involuntary muscle movements. Other motor symptoms are
possible including lip smacking.[14]
Early symptoms may include loss of precision muscle coordination (sometimes first manifested in
declining penmanship, frequent small injuries to the hands, and dropped items), cramping pain with
sustained use, and trembling. Significant muscle pain and cramping may result from very minor
exertions like holding a book and turning pages. It may become difficult to find a comfortable position
for arms and legs with even the minor exertions associated with holding arms crossed causing
significant pain similar to restless leg syndrome. Affected persons may notice trembling in
the diaphragm while breathing, or the need to place hands in pockets, under legs while sitting or
under pillows while sleeping to keep them still and to reduce pain. Trembling in the jaw may be felt
and heard while lying down, and the constant movement to avoid pain may result in the grinding and
wearing down of teeth, or symptoms similar to TMD. The voice may crack frequently or become
harsh, triggering frequent throat clearing. Swallowing can become difficult and accompanied by
painful cramping.[citation needed]
Electrical sensors (EMG) inserted into affected muscle groups, while painful, can provide a definitive
diagnosis by showing pulsating nerve signals being transmitted to the muscles even when they are
at rest. The brain appears to signal portions of fibers within the affected muscle groups at a firing

speed of about 10 Hz causing them to pulsate, tremble and contort. When called upon to perform an
intentional activity, the muscles fatigue very quickly and some portions of the muscle groups do not
respond (causing weakness) while other portions over-respond or become rigid (causing micro-tears
under load). The symptoms worsen significantly with use, especially in the case of focal dystonia,
and a "mirror effect" is often observed in other body parts: Use of the right hand may cause pain and
cramping in that hand as well as in the other hand and legs that were not being used. Stress,
anxiety, lack of sleep, sustained use and cold temperatures can worsen symptoms. [citation needed]
Direct symptoms may be accompanied by secondary effects of the continuous muscle and brain
activity, including disturbed sleep patterns, exhaustion, mood swings, mental stress, difficulty
concentrating, blurred vision, digestive problems, and short temper. People with dystonia may also
become depressed and find great difficulty adapting their activities and livelihood to a progressing
disability. Side-effects from treatment and medications can also present challenges in normal
activities.[citation needed]
In some cases, symptoms may progress and then plateau for years, or stop progressing entirely.
The progression may be delayed by treatment or adaptive lifestyle changes, while forced continued
use may make symptoms progress more rapidly. In others, the symptoms may progress to total
disability, making some of the more risky forms of treatment worth considering. In some cases with
patients who already have dystonia, a subsequent tramatic injury or the effects of general anethesia
during an unrelated surgery can cause the symptoms to progress rapidly.[citation needed]
An accurate diagnosis may be difficult because of the way the disorder manifests itself. Sufferers
may be diagnosed as having similar and perhaps related disorders includingParkinson's
disease, essential tremor, carpal tunnel syndrome, TMD, Tourette's syndrome, conversion
disorder or other neuromuscular movement disorders. It has been found that the prevalence of
dystonia is high in individuals with Huntington's disease, where the most common clinical
presentations are internal shoulder rotation, sustained fist clenching, knee flexion, and foot inversion.
[15]

Risk factors for increased dystonia in patients with Huntington's disease include long disease

duration and use of antidopaminergicmedication.[15]

Causes[edit]
Primary dystonia is suspected when the dystonia is the only sign and there is no identifiable cause
or structural abnormality in the central nervous system. It is suspected to be caused by a pathology
of the central nervous system, likely originating in those parts of the brain concerned with motor
function, such as the basal ganglia, and the GABA (gamma-aminobutyric acid) producing Purkinje
neurons. The precise cause of primary dystonia is unknown. In many cases it may involve some
genetic predisposition towards the disorder combined with environmental conditions. [citation needed]

Secondary dystonia refers to dystonia brought on by some identified cause, such as head injury[citation
, drug side effect (e.g. tardive dystonia), or neurological disease (e.g.Wilson's disease).

needed]

Meningitis and encephalitis caused by viral, bacterial, and fungal infections of the brain have been
associated with dystonia. The main mechanism is inflammation of the blood vessels, causing
restriction of blood flow to the basal ganglia. Other mechanisms include direct nerve injury by the
organism or a toxin, or autoimmune mechanisms.[16]
Environmental and task-related factors are suspected to trigger the development of focal dystonias
because they appear disproportionately in individuals who perform high precision hand movements
such as musicians, engineers, architects, and artists.[citation needed] Chlorpromazine can also cause
dystonia, which can be often misjudged as a seizure.[citation needed] Neuroleptic drugs often cause
dystonia, including oculogyric crisis.[citation needed]
Misfunction of the sodium-potassium pump may be a factor in some dystonias. The Na+
-K+
pump has been shown to control and set the intrinsic activity mode of cerebellarPurkinje neurons.
[17]

This suggests that the pump might not simply be a homeostatic, "housekeeping" molecule for

ionic gradients; but could be a computational element in thecerebellum and the brain. Indeed,
an ouabain block of Na+
-K+
pumps in the cerebellum of a live mouse results in it displaying ataxia and dystonia.[18] Ataxia is
observed for lower ouabain concentrations, dystonia is observed at higher ouabain concentrations. A
mutation in the Na+
-K+
pump (ATP1A3 gene) can cause rapid onset dystonia parkinsonism.[19]The parkinsonism aspect of
this disease is thought to be attributable to malfunctioning Na+
-K+
pumps in the basal ganglia; the dystonia aspect is thought to be attributable to malfunctioning Na+
-K+
pumps in the cerebellum (that act to corrupt its input to the basal ganglia) - possibly in Purkinje
neurons.[17]

Treatment[edit]
Reducing the types of movements that trigger or worsen dystonic symptoms provides some relief, as
does reducing stress, getting plenty of rest, moderate exercise, and relaxation techniques. [citation
needed]

Various treatments focus on sedating brain functions or blocking nerve communications with the

muscles via drugs, neuro-suppression, or denervation.[citation needed] All current treatments have negative
side-effects and risks.

Physical intervention[edit]
While research in the area of effectiveness of physical therapy intervention for dystonia remains
weak,[20] there is reason to believe that rehabilitation will benefit patients with dystonia. [21] Physical
therapy can be utilized to manage changes in balance, mobility and overall function that occur as a
result of the disorder.[22] A variety of treatment strategies can be employed to address the unique
needs of each individual. Potential treatment interventions include splinting, [23] therapeutic exercise,
manual stretching, soft tissue andjoint mobilization, postural training and bracing,[21] neuromuscular
electrical stimulation, constraint-induced movement therapy, activity and environmental modification,
and gait training.[22]
A patient with dystonia may have significant challenges in activities of daily living (ADL), an area
especially suited for treatment by occupational therapy (OT). An occupational therapist (OT) may
perform needed upper extremity splinting, provide movement inhibitory techniques, train fine motor
coordination, provide an assistive device, or teach alternative methods of activity performance to
achieve a patient's goals for bathing, dressing, toileting, and other valued activities.
Recent research has investigated further into the role of physiotherapy in the treatment of dystonia.
A recent study showed that reducing psychological stress, in conjunction with exercise, is beneficial
for reducing truncal dystonia in patients with Parkinsons Disease.[24] Another study emphasized
progressive relaxation, isometric muscle endurance, dynamic strength, coordination, balance, and
body perception, seeing significant improvements to patients quality of life after 4 weeks. [25]
Some focal dystonias have been proven treatable through movement retraining in the Taubman
approach, particularly in the case of musicians. However other focal dystonias may not respond and
may even be made worse by this treatment.
Due to the rare and variable nature of dystonia, research investigating the effectiveness of these
treatments is limited. There is no gold standard for physiotherapy rehabilitation.[24] To date, focal
cervical dystonia has received the most research attention; [22] however, study designs are poorly
controlled and limited to small sample sizes.[20]

Medication[edit]
Different medications are tried in an effort to find a combination that is effective for a specific person.
Not all people will respond well to the same medications. Medications that have had positive results

in some include: diphenhydramine, benzatropine, anti-Parkinsons agents (such

as trihexyphenidyl and bromocriptine), and muscle relaxants (such asdiazepam).
Anticholinergics
Medications such as anticholinergics (benztropine), which act as inhibitors of the
neurotransmitter acetylcholine, may provide some relief. In the case of an acute dystonic
reaction, diphenhydramine is sometimes used (though this drug is well known as an antihistamine, in
this context it is being used primarily for its anticholinergic role).[citation needed]. See also Procyclidine.
Baclofen
A baclofen pump has been used to treat patients of all ages exhibiting muscle spasticity along with
dystonia. The pump delivers baclofen via a catheter to the thecal space surrounding the spinal cord.
The pump itself is placed in the abdomen. It can be refilled periodically by access through the skin. [26]
Botulin toxin injection
Botulinum toxin injections into affected muscles have proved quite successful in providing some
relief for around 36 months, depending on the kind of dystonia. Botox injections have the
advantage of ready availability (the same form is used for cosmetic surgery) and the effects are not
permanent. There is a risk of temporary paralysis of the muscles being injected or the leaking of the
toxin into adjacent muscle groups, causing weakness or paralysis in them. The injections have to be
repeated, as the effects wear off and around 15% of recipients will develop immunity to the toxin.
There is a Type A and a Type B toxin approved for treatment of dystonia; often, those that develop
resistance to Type A may be able to use Type B.[27]
Muscle relaxants
Clonazepam, an anti-seizure medicine, is also sometimes prescribed. However, for most, their
effects are limited and side-effects like mental confusion, sedation, mood swings, and short-term
memory loss occur.[citation needed]
Parkinsonian drugs
Dopamine agonists: One type of dystonia, dopamine-responsive dystonia, can be completely treated
with regular doses of L-DOPA in a form such as Sinemet (carbidopa/levodopa). Although this does
not remove the condition, it does alleviate the symptoms most of the time. (In contrast, dopamine
antagonists can sometimes cause dystonia.)[citation needed]

Surgery[edit]
Surgery, such as the denervation of selected muscles, may also provide some relief; however, the
destruction of nerves in the limbs or brain is not reversible and should be considered only in the
most extreme cases. Recently, the procedure of deep brain stimulation (DBS) has proven successful
in a number of cases of severe generalised dystonia.[28] DBS as treatment for medication-refractory
dystonia, on the other hand, may increase the risk of suicide in patients. However, reference data of
patients without DBS therapy are lacking.[29]

See also[edit]

Vegetative-vascular dystonia
From Wikipedia, the free encyclopedia

It has been suggested that this article be merged into Dysautonomia.

(Discuss) Proposed since September 2014.
This article may be expanded with text translated from
the corresponding article in the Russian Wikipedia. (July 2013)
Click [show] on the right to read important instructions before translating.

[show]

Vegetative-vascular dystonia is a type of dystonia. It shares common features with

several autonomic dysfunctions, such as orthostatic hypotension and postural orthostatic
tachycardia syndrome. These features include orthostatic intolerance and vasovagal response.
Vegetative-vascular dystonia also has considerable overlap with other medical diagnoses,
including posttraumatic stress disorder, anxiety disorder, major depressive disorder, and somatoform
disorder. However, it is not formally recognized in existing ICD-9and ICD-10 disease classification
systems.
The closest analogue is autonomic dysfunction and mitral valve prolapse syndrome. [citation needed]
Characterization of vegetative-vascular dystonia in Western medical literature is limited. [1] However,
this disorder has been characterized extensively in Russian medical literature. [2][3][4][5][6] Until recently,
the (Russian) vegetative-vascular dystonia page incorrectly linked to Da Costa's
syndrome via Wikidata. However, a thorough description of this dystonia requires complete
translation of the Russian page into English and expansion of this English page on the subject.