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]
Spectrum of Disorders
editHypokinesia 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. |
Neurobiology
editHypokinetic symptoms arise from damage to the basal ganglia, which plays a role in producing force and computing the effort necessary to make a movement.[7] 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.[7]
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.[8] 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.[7]
Treatments
editTreatment for Parkinson’s Disease has involved the surgical destruction of the globus palidus internal, effectively activating the direct pathway in the basal ganglia and allowing for greater possibilities for muscle movement. [9]
Dopaminergic Drugs
editSome 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.[10]
Deep Brain Stimulation
editPosteroventral 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.[7]
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.[11] Patients are usually able to maintain normal levels of fluency, but often stop mid-sentence, unable to remember or produce a desired word.[11] 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.[12]
Stem Cells
editNew 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.[13] 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.[14]
Demographic Differentiation
editSymptoms
editStress 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.[15] Low-impact exercise, elimination of drug and alcohol use, and regular meditation can help to restore normal stress responses in hypokinesia patients.[16]
Connections to Other Medical Conditions
editThough 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.[17] |
| 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.[18] |
References
edit- ^ http://serendip.brynmawr.edu/bb/neuro/neuro03/web1/ljackson.html
- ^ Kolb, B. Whishaw, I. (2011) An Introduction to Brain and Behavior, 373.
- ^ Yorkston, Kathryn M. (June 2007). "Evidence for effectiveness of treatment of loudness, rate, or prosody in dysarthria: A systematic review". Journal of Medical Speech-Language Pathology. 15 (2): xi–xxxvi.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help)CS1 maint: date and year (link) - ^ a b Robottom, Bradley J. (1 May 2011). "Movement Disorders Emergencies Part 1". Archives of Neurology. 68 (5): 567–572. doi:10.1001/archneurol.2011.84. PMID 21555633.
- ^ Robottom, Bradley J. (9 May 2011). "Movement Disorders Emergencies Part 1<subtitle>Hypokinetic Disorders</subtitle>". Archives of Neurology. 68 (5): 567–572. doi:10.1001/archneurol.2011.84. PMID 21555633.
- ^ O'Sullivan, Susan B.; Schmitz, Thomas J. (2007). "Parkinson's Disease". Physical Rehabilitation. Vol. 5. Philadelphia: F.A Davis Company. pp. 856–857.
- ^ a b c d Whelan, Brooke-Mai; Murdoch, Bruce E.; Theodoros, Deborah G.; Silburn, Peter A.; Hall, Bruce (2005). "Borrowing from models of motor control to translate cognitive processes: Evidence for hypokinetic–hyperkinetic linguistic homologues?". Journal of Neurolinguistics. 18 (5): 361–381. doi:10.1016/j.jneuroling.2004.05.002. S2CID 53204203.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: date and year (link) - ^ Akbari, A. (23 September 2009). "Oscillations as the Cause of Both Hyper- and Hypokinetic Symptoms of Movement Disorders". Journal of Neuropsychiatry. 21 (3): 352. doi:10.1176/appi.neuropsych.21.3.352.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Kolb, B. Whishaw, I. (2011) An Introduction to Brain and Behavior, 375.
- ^ Louter, Maartje; Munneke, Marten; Bloem, Bastiaan R.; Overeem, Sebastiaan (2012). "Nocturnal Hypokinesia and Sleep Quality in Parkinson's Disease". Journal of the American Geriatrics Society. 60 (6): 1104–1108. doi:10.1111/j.1532-5415.2012.03966.x. PMID 22642534. S2CID 37852360.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: date and year (link) - ^ a b Alarcón, Fernando; Giménez-Roldán, Santiago (2005). "Systemic diseases that cause movement disorders". Parkinsonism & Related Disorders. 11 (1): 1–18. doi:10.1016/j.parkreldis.2004.10.003. PMID 15619457.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: date and year (link) - ^ CALIGIURI, M (April 1989). "The influence of speaking rate on articulatory hypokinesia in parkinsonian dysarthria*1". Brain and Language. 36 (3): 493–502. doi:10.1016/0093-934X(89)90080-1. PMID 2706450. S2CID 37280271.
{{cite journal}}: CS1 maint: date and year (link) - ^ Kolb, B. Whishaw, I. (2011) An Introduction to Brain and Behavior, 592.
- ^ Master, Z.; McLeod, M.; Mendez, I. (1 March 2007). "Benefits, risks and ethical considerations in translation of stem cell research to clinical applications in Parkinson's disease". Journal of Medical Ethics. 33 (3): 169–173. doi:10.1136/jme.2005.013169. PMC 2598267. PMID 17329391.
- ^ Grigor'Ev, A. I.; Fedorov, B. M. (1996 Mar-Apr). "Stress under normal conditions, hypokinesia simulating weightlessness, and during flights in space". Human Physiology. 22 (2): 139–47. PMID 11541518.
{{cite journal}}: Check date values in:|date=(help) - ^ Wolterink, G.; Van Ree, J. M. (1988 Mar-Apr). "Stress-induced hypokinesia is facilitated by ACTH-(7-10)". Peptides. 9 (2): 277–82. doi:10.1016/0196-9781(88)90260-4. PMID 2836824. S2CID 543154.
{{cite journal}}: Check date values in:|date=(help) - ^ Kim, E. J.; Lee, B.; Jo, M. K.; Jung, K.; You, H.; Lee, B. H.; Cho, H. J.; Sung, S. M.; Jung, D. S.; Heilman, K. M.; Na, D. L. (2013 Jul). "Directional and spatial motor intentional disorders in patients with right versus left hemisphere strokes". Neuropsychology. 27 (4): 428–37. doi:10.1037/a0032824. PMID 23876116.
{{cite journal}}: Check date values in:|date=(help) - ^ Bracht, T (2013 Feb). "Altered cortico-basal ganglia motor pathways reflect reduced volitional motor activity in schizophrenia". Schizophrenia Research. 143 (2–3): 269–76. doi:10.1016/j.schres.2012.12.004. PMID 23276479. S2CID 20131894.
{{cite journal}}: Check date values in:|date=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help)