What is Akinesia?
Akinesia is a compound word that comes from the prefix, “-a”, meaning without or lacking thereof and, the Greek word “kinesis”, meaning movement or in motion. Literally speaking, akinesia translates to “the lacking of movement” or “without movement”. It is also widely dubbed as “poverty in movement”.
In the medical field, particularly in neurology however, a more specific definition of akinesia would be the inability or incapability to initiate a particular act of motion. Basically, akinesia is a motor disorder.
Causes of Akinesia
Generally speaking, akinesia occurs due to a problem in the nervous system, which concerns a particular trouble in picking and/or setting a particular motor program in motion. This trouble may be caused by various factors such as the following:
- A trauma in the frontal lobe, which is the primary movement control center; and
- Several underlying and associated conditions that trigger the manifestation of akinesia as discussed in a separate section below.
Signs and Symptoms Of Akinesia
More often than not, patients with akinesia are apathetic in nature. Meaning, the patient is indifferent and generally, there is absence of interest in the external environment. In addition, there is obviously a diminished or significant reduction in movement, especially in the patient’s ability for spontaneous ones. The patient may also be rendered immobile. Talking about the patient’s face, they are mostly expressionless and their faces appear fixed.
Blinking of the eyelids is rare and the patient’s way of speech is generally monotonous with accompanying absence of modulation. The patient may also be easily fatigued if posed to do repetitive movements. Furthermore, there is also inability to perform otherwise normal tasks such as simultaneous and sequential actions.
Akinesia as a part of extrapyramidal symptoms (EPS)
Extrapyramidal symptoms are physical side effects of anti-psychotic medications used to treat schizophrenia. An example of such anti-psychotic drug is Haloperidol (Haldol).
Extrapyramidal symptoms occur when the control of the extrapyramidal system is altered or disturbed. This alteration is due to the blockage of dopamine, which primarily controls the exptrapyramidal system. However, anti-psychotic drugs block this dopamine in an effort to significantly reduce dopamine levels to treat schizophrenia.
Aside from akinesia, other cardinal symptoms of EPS are dystonia or involuntary contractions of the muscle, akathisia or restlessness, pseudoparkinsonism, neuroleptic malignant syndrome and tardive dyskinesia (which is late appearing and irreversible in nature).
Akinesia as a symptom of Parkinson’s disease
Parkinson’s disease is a neurologic movement disorder that is slowly progressive in nature and may consequently lead to disability. Furthermore, it is characterized by the decreased ability of the brain to coordinate all the body’s motor activities. The cause of Parkinson’s disease is either idiopathic (unknown) in nature or with a suspected underlying cause.
Moving on, akinesia is one of the most common characteristics or symptoms of Parkinson’s disease. It is caused by a reduction in the levels of dopamine in the body, which is a direct effect of the damage of certain pigmented neuronal cells located in the substantia nigra of the brain’s basal ganglia region. Dopamine is an inhibitory transmitter, hence the lack of or diminished level of it in the body may cause an imbalance between inhibitory neurotransmitters and those excitatory ones (acetylcholine). This imbalance may in turn, cause a signifcant disturbance in voluntary movement such as akinesia.
As an added tidbit of information, Parkinson’s disease is a widely known condition that affected Muhammad Ali, one of the most acclaimed athletes in history.
Akinetic Crisis
Akinetic crisis occurs in patients with Parkinson’s disease who are subjected to long-term therapy with levo-dihydroxyphenylalanine or L-DOPA. Essentially, akinetic crisis is typified by severe disability to move. Administration of iron in the form of ferri-ferro-complex through intravenous route has resulted into significant alleviation of the akinetic crisis with patients regaining a considerable ability to move.
The alleviation of the crisis is however dependent on the dosage administered. Fundamentally, the larger the dose, the more significant changes and/or improvement can occur. However, it is very important to assess the condition of the patient first before deciding on the dosage to be administered as several factors should also be considered. Furthermore, tapering or withdrawing the iron administration should be handled or managed carefully as improper withdrawal may trigger the relapse of an akinetic crisis.
Akinetic Mutism
Akinetic mutism is characterized by two distinct conditions, which are the inability to move (akinesia) and inability to speak (mutism). Akinetic mutism occurs due to a trauma in the frontal lobe, which is responsible for the control of motor functions. A trauma in the frontal lobe may be attributed to cases of encephalitis lethargica, Creutzfeldt-Jakob disease, olfactory groove meningioma, stroke and drug related causes such as neurotoxicity brought about by cyclosporine.
Fetal Akinesia
Fetal akinesia is characterized by a total lack of fetal movement. This total lack of fetal movement is due to a number of disorders that ultimately results to the inability to initiate movement or akinesia. These disorders include camptodactyly, rocker-bottom feet, ulnar deviation of the hands, facial anomalies, multiple joint contractures and pulmonary hypoplasia among others.
Almost one-third of the cases are stillborn and a high percentage of the infants who are alive upon delivery, die shortly after birth, primarily due to the complications imposed by pulmonary hypoplasia. Moreover, half of the known cases show an autosomal recessive inheritance that may recur in siblings and/or with parental consanguinity.
Pure akinesia
Pure akinesia is characterized by pulsion symptoms with the absence of tremor and rigidity. Moreover, it is also typified by the freezing of gait. Pure akinesia is furthermore, non-responsive to levodopa therapy.
In recent studies, pure akinesia has been linked to a condition called progressive supranuclear palsy otherwise known as Steele-Richardson-Olszewski syndrome as one of its atypical manifestations. Other accompanying symptoms of pure akinesia are nuchal rigidity, supranuclear ophthalmoplegia, pseudobulbar palsy and dementia.
Other diseases associated with akinesia
Akinesia may manifest in other various diseases such as the following:
- Huntington’s disease – Huntington’s disease is a disease involving the degeneration of nerve cells, which is genetic or hereditary in nature. Akinesia appears in people who develop Huntington’s disease in their adult age without accompanying chorea. These patients appear rigid most of the time and moves very little or not at all.
- Multiple pterygium syndrome – Multiple pterygium syndrome occurs due to the mutation in the gene called CHRNG. It is transmitted through an autosomal recessive pattern and is typified by the occurrence of webbing in the skin at the joints (pterygium) and a lack of movement (akinesia).
- Corticobasal degeneration – Corticobasal degeneration is a neurologic disorder that is generally progressive in nature. It affects several regions of the brain including the basal ganglia and the cerebral cortex respectively. Akinesia, along with impaired balance, limb dystonia, disturbance in equilibrium, apraxia or the inability to do purposeful movements, dysphagia or the difficulty in swallowing and muscle rigidity are its most characteristic symptoms.
Akinesia Treatment
Medical Management
The medical management of a patient affected by akinesia should be jointly discussed by the attending physician and his/her significant others. It is important to keep the significant others in the loop to provide optimal care to the patient.
Pharmacologic Therapy
There are a number of pharmacologic therapies utilized to treat or alleviate akinesia. Some of which are as follows:
- Levodopa – Levodopa is a peripheral decarboxylase inhibitor or PDI. Through the years, Levodopa has been the most common and single most effective medication used to treat associated impairments brought about by Parkinson’s disease and its associated symptoms such as akinesia.
- L-DOPS (L-threo-dihydroxypheny
lserine; Droxidopa) – This drug has been proven beneficial to patients with pure akinesia. The micrographia as well as apraxia of opening the eyelid and frozen gait present in patients with pure akinesia has been significantly improved. - Dopamine agonists – This drug claims to be beneficial in treating akinesia. It is said that akinesia occurs due to the rapidly dwindling dopaminergic cell activity in the direct movement pathway. This drug acts by directly stimulating the dopamine receptors present in the brain. Hence, the administration of a therapeutic level of dopamine agonists in the body at certain hours of the day may help in the resolution of akinesia. Examples of dopamine agonists are Parlodel, Requip and Neupro respectively.
For added information, there have been research studies regarding intranigral or intracerebroventricular injection of GABA in reserpine-treated rat that shows reversal of akinesia.
Supportive Care
Individuals affected with akinesia are at a high risk for falls resulting to serious injuries, especially in cases of pure akinesia. Hence, thorough supportive care should be provided to these patients. To prevent falls, it is imperative to watch the patient at all times. However, in cases where it is necessary to leave the patient out of sight, it is important to raise the bed’s side rails at all times.
Physical Therapy
There have been physical therapies specially designed to provide symptomatic relief for akinesia in patients with Parkinson’s disease. In a particular research study, patients with akinesia who train in a rotating treadmill following a set of procedures report to show normalization in the muscle activity and lesser episodes of freezing in movement when turning.
References
http://www.ncbi.nlm.nih.gov/
