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| Hypokinesia | |
|---|---|
| Classification and external resources | |
| MeSH | D018476 |
Hypokinesia refers to decreased bodily movement.[1] One of the two categories of movement disorders, hypokinesia is characterized by a partial or complete loss of muscle movement due to a disruption in the basal ganglia. Patients with hypokinetic disorders like Parkinson’s Disease experience muscle rigidity and an inability to produce movement. It is also associated with mental health disorders and prolonged inactivity due to illness, amongst other diseases.
The other category of movement disorder resulting from damage to the basal ganglia, hyperkinesia, features an exaggeration of unwanted motion, like twitching or writhing in Huntington’s disease or Tourette's Syndrome.[2]
Contents
- 1 Spectrum of Disorders
- 2 Pathophysiology
- 2.1 Associated Neurotransmitters
- 2.2 Neurobiology
- 3 Treatments
- 3.1 Dopaminergic Drugs
- 3.2 Deep Brain Stimulation
- 3.3 Methylphenidate
- 3.4 Stem Cells
- 3.5 NOP Receptor Antagonists
- 3.6 Dance Therapy
- 4 Associations
- 4.1 Cognitive Impairment
- 4.2 Motor Motivation
- 4.3 Demographic Differentiation
- 4.4 Symptoms
- 5 Connections to Other Medical Conditions
- 6 See also
- 7 References
Spectrum of Disorders
Hypokinesia describes a variety of more specific disorders:
| Hypokinetic Disorder | Characteristics |
|---|---|
| Akinesia (α- a-, "without", κίνησις kinēsis, "motion") | Inability to initiate movement due to difficulty selecting and/or activating motor programs in the central nervous system. Common in severe cases of Parkinson's disease, akinesia is a result of severely diminished dopaminergic cell activity in the direct pathway of movement. |
| Bradykinesia (βραδύς bradys, "slow", κίνησις kinēsis, "motion") | Characterized by slowness of movement and has been linked to Parkinson's disease and other disorders of the basal ganglia. Rather than being a slowness in initiation (akinesia), bradykinesia describes a slowness in the execution of movement. It is one of the 4 key symptoms of parkinsonism, which are bradykinesia, tremor, rigidity and postural instability. Bradykinesia is also the cause of what is normally referred to as "stone face" (expressionless face) among those with Parkinson's. |
| Dysarthria | A condition which affects the muscles necessary for speech, causing difficulty in speech production despite a continued cognitive understanding of language. Often caused by Parkinson's disease, patients experience weakness, paralysis or lack of coordination in the motor-speech system, causing respiration, phonation, prosody, and articulation to be affected. Problems ranging from tone, speed of communication, breath control, volume and timing are displayed. Hypokinetic dysarthria particularly affects the volume of speech, prompting treatment with a speech language pathologist.[3] |
| Dyskinesia | Characterized by a diminished ability for voluntary movements as well as the presence of involuntary movements. The hands and upper body are the areas most likely to be affected by tremors and tics. In some cases, Parkinson's patients experience dyskinesia as a negative side effect of dopamine medications.[4] |
| Dystonia | Patients experience muscle twisting, repetition and abnormal postures. The disease could be caused by genetics or a variety of environmental factors such as reaction to drugs or birth-related trauma.[5] |
| Freezing | Characterized by an inability to move muscles in any desired direction. |
| Neuroleptic malignant syndrome | Results from heavy exposure to drugs that block dopamine receptors. Victims can experience fever, rigidity, mental status change, dysautonomia, tremors, dystonia and myoclonus. While this disorder is extremely rare, immediate attention is necessary because of the high risk of death.[4] |
| Rigidity | Characterized by an increase in muscle tone causing resistance to externally imposed joint movements.[6] It does not depend on imposed speed and can be elicited at very low speeds of passive movement. It is felt in both agonist and antagonist muscles and in movements in both directions. 'Cogwheel' rigidity and 'leadpipe' rigidity are two types identified with Parkinson's disease. 'Leadpipe' rigidity results when an increase in muscle tone causes a sustained resistance to passive movement throughout the whole range of motion, with no fluctuations. 'Cogwheel' rigidity is a combination of leadpipe rigidity and tremor which presents as a jerky resistance to passive movement as muscles tense and relax. Spasticity is a special form of rigidity that is present only at the start of passive movement. It is rate dependent and only elicited upon a high speed movement. These various forms of rigidity can be seen in different forms of movement disorders, such as Parkinson's disease. |
| Postural instability | Loss of ability to maintain an upright posture. |
A person with medication induced dystonia.
Pathophysiology
Associated Neurotransmitters
Dopamine
The main neurotransmitter thought to be involved in hypokinesia is dopamine.[7][8] Essential to the basal ganglionic-thalamo-cortical loop, which processes motor function, dopamine depletion is common in these areas of hypokinesic patients.[8] Bradykinesia is correlated with lateralized dopaminergic depletion in the substantia nigra.[8] The dopamine pathway in the substantia nigra is essential to motor function, and commonly a lesion in this area correlates with displayed hypokinesia.[8][9] Tremor and rigidity, however, seem to be only partially due to dopamine deficits in the substantia nigra, suggesting that there are other processes involved in motor control.[8] Treatments for hypokinesia often either attempt to prevent dopamine degradation by MAO-B or increase the amount of neurotransmitter present in the system.[8][9]
GABA and Glutamate
The inhibitory neurotransmitter GABA and the excitatory glutamate are found in many parts of the central nervous system, including in the motor pathways that involve hypokinesia. In one pathway, glutamate in the substantia nigra excites the release of GABA into the thalamus, which then inhibits the release of glutamate in the cortex and thereby reduces motor activity. If there is too much glutamate initially in the substantia nigra, then through interaction with GABA in the thalamus and glutamate in the cortex, movements will be reduced or will not occur at all.[10]
Another direct pathway from the basal ganglia sends GABA inhibitory messages to the globus pallidus and substantia nigra, which then send GABA to the thalamus. In the indirect pathway the basal ganglia sends GABA to the globus pallidus which then sends it to the subthalamic nucleus, which then disinhibited sends glutamate to the output structures of the basal ganglia. Inhibition of GABA release could disrupt the feedback loop to the basal ganglia and produce hypokinesic movements.[11]
GABA and glutamate often interact with each other and with dopamine directly. In the basal ganglia, there is a nigrostriatal pathway where GABA and dopamine are housed in the same neurons and released together.[12]
Neurobiology
Hypokinetic symptoms arise from damage to the basal ganglia, which plays a role in producing force and computing the effort necessary to make a movement.[13] There are two possible neural pathways enabling the basal ganglia to produce movement. When activated, the direct pathway sends sensory and motor information from the cortex to the first structure of the basal ganglia, the putamen. That information directly inhibits the globus pallidus internal and allows free movement. The indirect pathway, traveling through the putamen, globus pallidus external, and subthalamic nucleus, activates the globus pallidus internal threshold and inhibits the thalamus from communicating with the motor cortex, producing hypokinetic symptoms.[13]
Basal Ganglia and Related Structures
When levels of dopamine decrease, the normal wave firing pattern of basal ganglia neural oscillations changes and the tendency for oscillations increases, particularly in the beta wave of the basal ganglia.[14] Recent research indicates that when oscillations fire simultaneously, processing is disrupted at the thalamus and cortex, affecting activities such as motor planning and sequence learning as well as causing hypokinetic tremors.[13]
Treatments
Dopaminergic Drugs
Dopaminergic drugs are commonly used in the early stages of the hypokinesia to treat patients.[9] However, with increased intake they can become ineffective because of the development of noradrenergic lesions.[9] While initially the dopaminergic drugs may be effective, these noradrenergic lesions are associated with hypokinesic gait disorder development later on.[8][9]
Some Parkinson's patients are unable to move during sleep, prompting the diagnosis of "nocturnal hypokinesia." Physicians have experienced success treating this sleep disorder with slow-release or night-time dopaminergic drugs, and in some cases, continuous stimulation by the dopamine agonist rotigotine. Despite improved mobility during sleep, many Parkinson's patients report an extremely uncomfortable sleeping experience even after dopaminergic treatments.[15]
Deep Brain Stimulation
Once the reaction to dopaminergic drugs begins to fluctuate in Parkinson’s patients, Deep Brain Stimulation (DBS) of the subthalamic nucleus and medial globus pallidus is often used to treat hypokinesia.[9][16][17] DBS, like dopaminergic drugs, initially provides relief but chronic use causes worse hypokinesia and freezing of gait.[9][18] Lower frequency DBS in non-regular patterns has been shown to be more effective and less detrimental in treatment.[17][18]
Parkinson surgery
Posteroventral pallidotomy (PVP) is a specific kind of deep brain stimulation that destroys a small part of the globus pallidus by scarring the neural tissue, reducing brain activity and therefore tremors and rigidity. It is suspected that PVP recalibrates basal ganglia activity in the thalamocortical pathway. PVP in the dominant hemisphere has been reported to disrupt executive function verbal processing abilities, and bilateral PVP may disturb processes of focused attention.[13]
Many akinesia patients also form a linguistic akinesia in which their ability to produce verbal movements mirrors their physical akinesia symptoms, especially after unsuccessful PVP deep brain stimulation.[19] Patients are usually able to maintain normal levels of fluency, but often stop mid-sentence, unable to remember or produce a desired word.[19] According to a study of Parkinson's patients with articulatory hypokinesia by Caligiuri (1989), subjects with faster rates of speech experienced more problems trying to produce conversational language than those who normally spoke at slower rates.[20]
Methylphenidate
Methylphenidate, commonly used to treat ADHD, has been used in conjunction with levodopa to treat hypokinesia in the short-term.[9] The two work together to increase dopamine levels in the striatum and prefrontal cortex.[9] Methylphenidate mainly inhibits dopamine and noradrenaline reuptake by blocking presynaptic transporters and levodopa increases the amount of dopamine, generally improving hypokinesic gait.[9][21] Some patients, however, have adverse reactions of nausea and headache to the treatment and the long-term effects of the drug treatment still need to be assessed.[9]
Stem Cells
New treatments include increasing the number of dopamine cells by transplanting stem cells into the basal ganglia or stimulating endogenous stem cell production and movement to the basal ganglia.[22] The successful integration of stem cells can relieve hypokinetic symptoms and decrease the necessary dosage of dopaminergic drugs. However, a variety of complications, including possible tumor formation, inappropriate cell migration, rejection of cells by the immune system and cerebral hemorrhage are possible, causing many physicians to believe that the risks outweigh the possible benefits.[23]
NOP Receptor Antagonists
Another treatment that is still in an experimental stage is the administration of nociception FQ peptide (NOP) receptor antagonists. This treatment has been shown to reduce hypokinesia in animal studies when increasing nociception FQ in the substantia nigra and subthalamic nucleus. Low doses can be taken with dopaminergic treatment to decrease the amount of L-dopa needed, which can reduce its long-term side effects and improve motor performance.[24]
Dance Therapy
Dance therapy has also been shown to reduce hypokinesic movements and rigidity, though targeted more at the muscular aspects of the disorder than the neural activity.[25]
Associations
Cognitive Impairment
Bradykinesia has been shown to precede impairment of executive functions, working memory, and attention.[7][26] These cognitive deficiencies can be tied to non-function of the basal ganglia and pre-frontal cortex, which is also linked to the motor-dysfunction of hypokinesia.[7] Tremor and rigidity have not had observable connections to cognitive impairments, supporting the idea that they are not as involved in the dopamine pathway in the basal ganglionic-thalamo-cortical loop.[7][8] Dopaminergic treatments have shown improvement in cognitive functions associated with hypokinesia, suggesting they are also dependent on dopamine levels in the system.[26]
Motor Motivation
Often debated is whether the efficiency, vigor, and speed of movements in patients with hypokinesia are tied to motivation for rewarding and against punishing stimuli. The basal ganglia has been tied to the incentives behind movement, therefore suggesting that a cost/benefit analysis of planned movement could be affected in hypokinesia. Interestingly, rewards have not been shown to change the aspects of a hypokinesic individual’s movement.[27] In fact, the motor planning and control of a patient with hypokinesia is already as efficient as possible (as shown by slightly faster but generally the same movement after deep brain stimulation of the subthalamic nucleus).[28] This suggests that hypokinetic individuals simply have a narrower range of movement that does not increase relative to motivation.[27][29]
Other studies have come to the same conclusion about rewards and hypokinesia but have shown that aversive stimuli can, in fact, reduce hypokinesic movement. Shiner et al., in their assessment of this finding, suggest that dopamine is either less involved or has a more complex role in the response to punishment than it does to rewards, as the hypodopaminergic striatum allows more movement in response to aversive stimuli.[30]
Demographic Differentiation
Gender
More men than women typically develop hypokinesia, which is reflected in young and middle aged populations where females have displayed higher levels of nigrostriatal dopamine than males. In the elderly, however, this differentiation is not present. Typically, women exhibit more tremor in the beginning development of hypokinesia. In the disorder, men tend to display more rigidity and women more bradykinesic motor behavior, though this is not true in all cases.[31]
Age of Onset
Hypokinesia is displayed in the brain and outwardly slightly different depending on when an individual is first affected. In young-onset hypokinesia (younger than 45 years of age), there is typically slightly more cell loss in the substantia nigra and more displayed dystonia and muscle stiffness. In old-onset hypokinesia (older than 70 years of age), there is typically more of a hypokinesic gait and difficulty walking and no dystonia. Both onsets can display resting tremor, although more generally found in old-onset cases.[32]
Symptoms
Stress causes alterations of cerebral circulation, increasing blood flow in the supramarginal gyrus and angular gyrus of the parietal lobe, the frontal lobe and in the superior temporal gyrus of the left hemisphere. There is also an increase in cardiac activity and change in the tonus of the heart vessels, which is an elementary indication of stress development. In patients with normal stress, an adaptive fight-or-flight response is usually triggered by sympathetic nervous system activation. Hypokinesia patients experience these typical stress symptoms on a regular basis because of damage to the basal ganglia system. Therefore, when a hypokinesia victim is under stress, he or she does not display a typical fight-or-flight response, placing the patient under greater danger from potentially harmful stimuli.[33] Low-impact exercise, elimination of drug and alcohol use, and regular meditation can help to restore normal stress responses in hypokinesia patients.[34]
Connections to Other Medical Conditions
Though it is often most associated with Parkinson's disease, hypokinesia can be present in a wide variety of other conditions.
| Condition | Connection to Hypokinesia |
|---|---|
| Stroke | Damage to certain areas of the brain due to lack of oxygenation has been found to cause hypokinetic symptoms. Frontal and subcortical lesions caused by stroke are more likely to cause hypokinesia than posterior lesions.[35] |
| Schizophrenia | The lack of connections between the right supplementary motor area to the pallidum and the left primary motor cortex to the thalamus shown in patients with schizophrenia is thought to lead to hypokinesia.[36] |
| Hyperammonemia | Chronic hyperammonemia and liver disease can alter neurotransmission of GABA and glutamate by increasing the amount of glutamate in the substantia nigra and inhibiting movement.[10] |
| Progressive supranuclear palsy | Very similar to Parkinson’s disease, supranuclear palsy does not actually display the hypokinetic characteristic of progressive loss of movement, despite small amplitude. Diagnosis of hypokinesia can help to distinguish this disorder from Parkinson’s.[21] |
See also
- Akinetic mutism
- Hypokinetic diseases
- Hyperkinesia
References
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UpToDate Contents
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- 1. パーキンソン病における症状の変動およびジスキネジア motor fluctuations and dyskinesia in parkinson disease
- 2. 遅発性ジスキネジア：臨床的特徴および診断 tardive dyskinesia clinical features and diagnosis
- 3. 進行性核上性麻痺（PSP） progressive supranuclear palsy psp
- 4. 眼の待機手術に対する麻酔 anesthesia for elective eye surgery
- 5. 大脳皮質基底核変性症 corticobasal degeneration
English Journal
- Extrapyramidal adverse drug reactions associated with trimetazidine: a series of 21 cases.
- Masmoudi K, Masson H, Gras V, Andréjak M.SourceUnité de Neurologie-Neuropharmacovigilance, Service de Pharmacologie Clinique, CHU Amiens, France Centre Régional de Pharmacovigilance, Service de Pharmacologie Clinique, CHU Amiens, France Inserm ERI 12, Amiens, France.
- Fundamental & clinical pharmacology.Fundam Clin Pharmacol.2012 Apr;26(2):198-203. doi: 10.1111/j.1472-8206.2011.01008.x. Epub 2011 Nov 2.
- Over the last few years, a number of cases of extrapyramidal disorders associated with trimetazidine (TMZ) use has been reported. Here, we report on a series of 21 cases. All but one of the patients (mean age 74) had been taking TMZ for several years. The indication for prescription of TMZ could not
- PMID 22044594
- Sleep disorders in Parkinson's disease: Many causes, few therapeutic options.
- Diederich NJ, McIntyre DJ.SourceDepartment of Neurosciences, Centre Hospitalier de Luxembourg, 4, rue Ernest Barblé, Luxembourg-City, L-1210, Luxembourg; Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Campus Belval, 7, avenue des Hauts-Fourneaux. L-4362 Esch-sur-Alzette, Luxembourg.
- Journal of the neurological sciences.J Neurol Sci.2012 Mar 15;314(1-2):12-9. Epub 2011 Nov 25.
- Sleep symptoms in Parkinson's disease (PD) are frequent and have multifactorial and multilayered causes. Primary involvement of sleep/wake regulating centers in the brainstem, sleep problems caused by the nocturnal manifestation of motor and dysautonomic signs and medication-induced sleep problems a
- PMID 22118862
Japanese Journal
- 症例報告 緩徐な進行で長期経過を呈した進行性核上性麻痺の1剖検例
- 岩崎 靖,森 恵子,伊藤 益美
- 臨床神経学 52(3), 156-160, 2012-03
- NAID 40019232476
- A case of Wilson disease treated as schizophrenia for 20 years
- 久米井 伸介,柴田 道彦,本間 雄一,松橋 亨,日浦 政明,大西 裕,阿部 慎太郎,田原 章成,原田 大
- 肝臓 53(12), 2012
- … Later, he presented with difficulty in walking and akinesia like drug-induced parkinsonism. …
- NAID 130003343865
Related Links
- akinesia 【名】《病理》無動（症） - アルクがお届けするオンライン英和・和英辞書検索サービス。 もう英文作成で悩まない！120万例文と用例の「Pro」 データ提供：EDP 悪質な拡張機能にご注意ください データ投稿 ガイド 環境設定 ...
- akinesia Neurology Absent or decreased voluntary movement. Pharmacology Temporary paralysis of a muscle by procaine injection. Psychiatry Hysterical paralysis, see there. akinesia Neurology Absent or ↓ voluntary movement ...
- 世界大百科事典 第2版 - akinesiaの用語解説 - 過動症にはこのほか，アテトーシスやジストニーなどがあるが，いずれも意志の力では止めることのできない異常運動である。一方，同じ大脳基底核の病変でも，黒質や淡蒼球がおかされると ...
Related Pictures
★リンクテーブル★
| リンク元 | 「パーキンソン病」「無動」「瞬目麻酔」「無動症」「アキネジア」 |
「パーキンソン病」
- 英
- Parkinson disease Parkinson's disease PD
- 同
- Parkinson病
- 振戦麻痺 paralysis agitans shaking palsy、特発性パーキンソニズム idiopathic parkinsonism
- 関
- 症候性パーキソニズム、定位脳手術
疫学
- 50-60歳のに発症
- 有病率は10万人対約100人
病因
- 不明
病理
- 黒質線条体系のドーパミン欠如が成因に関与している (SPC.9)
- 黒質緻密部メラニン含有細胞の変性萎縮減少と残像神経細胞の細胞内にレビー小体が出現する。レビー小体 Lewy小体
- 障害部位およびレビー小体の出現部位：黒質緻密部、迷走神経背側運動核、交感神経心臓枝の節後線維、嗅球、青斑核、縫線核、マイネルト基底核、扁桃核。 (HBN.938)
- 時にレビー小体が大脳皮質に出現。(HBN.938)
病態生理
- at 黒質
- 脳の神経細胞は加齢により減少。
- パーキンソン病では減少が早く著しい
- ↓
- 黒質ドパミン神経細胞が変性脱落し、ドパミンを十分合成できない。
- 線条体コリン神経が優位
症状
- 1. 運動症状 3大徴候
- 安静時振戦 rest tremor
- 固縮 rigidity
- 無動 akinesia ← 動作緩慢 bradykinesia と記述される場合もある (HIM.2550)
- 姿勢保持反射障害 postual instability
- 2. 精神障害 認知症、うつ病、神経心理学障害
- 3. 自律神経障害 便秘、起立性低血圧、流涎(ﾘｭｳｾﾞﾝ)、排尿障害、脂漏
症状の頻度
- 振戦 58.2%
- 歩行障害 24.0%
- 動作緩慢 20.9%
症状の初発
- 振戦 ＞ 歩行障害、固縮、無動
- すくみ足や姿勢反射障害で発症することはない
病因
- 若年性Perkinson病、家族性慢性優性遺伝型Perkinson病
- 1. Parkin遺伝子の異常、1998年
- chr6にあるパーキン遺伝子の変異
- パーキンはユビキチンリガーゼの一種
- パーキンの変異でパエル受容体が異常蓄積
- 2. α-synclein遺伝子の異常、1998年
- chr4上のα-synuclein gene
- リン酸、αシヌクレイン異常蓄積
- ドパミン神経細胞師を引き起こす
- 薬剤性：黒質線条体ドーパミン神経の脱落
- 除草剤パラコート、園芸用殺虫剤マンネブ、天然系殺虫剤ロテノン
治療
薬物療法
薬物治療の副作用
- wearing-off phenomenon：レボドパによって生じる
脳深部刺激療法
その他
症状
- these various motor impediments and tremors characteristically begin in one limb (more often the left) and spread to one side and later to both sides until the patient is quite helpless.(APN.1036) 片側性で始まる
国試
「無動」
「瞬目麻酔」
- 眼科手術時に顔面神経をブロックすることにより眼瞼の緊張を取り、閉瞼不能にするための麻酔法。
「無動症」
「アキネジア」
- 英
- akinesia
- 運動不能、無動