NEUR3101 Motor Control Lecture 21: Stroke and Rehabilitation PDF

NEUR3101 Motor control Lecture 21 Stroke and rehabilitation A/Prof Ingvars Birznieks  Learning Outcomes You should be able to: Describe the general consequences for movement control of upper motor neuron (UMN) syndromes Explain the common symptoms and t...

NEUR3101 Motor control Lecture 21 Stroke and rehabilitation A/Prof Ingvars Birznieks  Learning Outcomes You should be able to: Describe the general consequences for movement control of upper motor neuron (UMN) syndromes Explain the common symptoms and typical motor dysfunctions associated with stroke Identify recovery mechanisms after stroke Understand aims of rehabilitation programs In addition, this lecture will reinforce your understanding of the role of the descending tracts in the control of movement by appreciating the problems caused by the loss of input or nervous tissue damage. Consequences of diminished descending control of spinal motor neurons While input from the upper motor neurons essential for initiation of voluntary movements is excitatory, the majority of inputs controlling spinal reflexes are inhibitory supressing reflexes when they are not meaningful. The major inhibitory system originates from ventromedial bulbar reticular formation and runs via the dorsal reticulospinal tract. It is activated by the premotor cortex. If premotor cortex is damaged, the inhibition is removed. The excitatory counterpart is dorsal reticular formation which is not under direct cortical control and thus remains active after cortical damage. Thus the reduction in descending inhitory input to spinal interneurons result in exaggerated unrestricted flow of excitation reaching motor neurons. Also the intrinsic motoneuron excitability may increase to compensate for the reduction of functional activation of the spinal cord.  Signs and symptoms of UMN dysfunction … due to disinhibition of spinal reflexes hyperreflexia - exaggerated reflexes spasticity - muscular hypertonicity with increased tendon reflexes; unlike rigidity it is velocity dependant, i.e., the faster the muscle is stretched the greater resistance and more reflex activity; affects movement in one direction (usually antigravity muscles) https://youtu.be/gLZoYLxdXCQ (rigidity)* - an increased muscle tone leading to a resistance to passive movement throughout the range of motion in both directions. Residual muscle tone or tonus is partial contraction of the muscles during resting state. It is present in normal muscle. * NOTE: Rigidity is not a typical sign of UMN damage, rather it results from dysregulation of UMN function originating from the basal ganglia. clasp-knife phenomenon - a manifestation of corticospinal spasticity in which there is sudden release of the resistance to passive flexion/extension typically near the end of the range of joint movement https://youtu.be/re0WKy1zlY0 clonus – muscular spasm involving a series of brisk repeated rhythmic, monophasic (i.e., unidirectional) contractions and relaxations of a group of muscles https://youtu.be/UX75k8s5QUE myoclonus - very rapid, shock-like contraction(s) of a group of muscles, which are irregular in rhythm and amplitude  Signs and symptoms of UMN damage … due to disinhibition of spinal reflexes (continued) contracture - a permanent structural shortening of a muscle or joint usually in response to prolonged hypertonic spasticity producing deformity Babinski sign - reversal of cutaneous flexor reflex … due to lost voluntary control loss of dexterity slowness, and clumsiness Reversal of cutaneous flexor reflex Babinski sign The Babinski sign. Following the removal of descending corticospinal pathways, stroking the sole of the foot may cause an abnormal fanning of the toes and the extension of the big toe (positive Babinski sign). It is used as a diagnostic tool.  Reversal of cutaneous flexor reflex Babinski sign Infants will also show an extensor response. A baby's smaller toes will fan out and his big toe will dorsiflex slowly. This happens because the corticospinal pathways that run from the brain down the spinal cord are not fully myelinated at this age, so the reflex is not inhibited by the cerebral cortex. The extensor response disappears and gives way to the flexor response around 12 to 24 months of age. Signs of loss of UMN and LMN function Summary Lost input from the Lost input from the Upper motor neurons (UMN) Lower motor neurons (LMN) Spasticity and tone Increased, with ‘clasp knife’ quality Decreased Clonus Present Absent Fasciculations* Absent Present Absent, but disuse atrophy Muscle wasting eventually results Present Tendon reflexes Increased Decreased or absent Extensor plantar reflexes Flexor plantar reflexes Babinski sign (Positive) weak or not present Wider effects, but proximal muscles affected less. Weakness is more apparent in the upper limb extensors Specific muscle groups and lower limb flexors simply Distribution affected (e.g. in the distribution reflecting natural strength of of a spinal segment) muscles (note: UMN damage affects flexors and extensors equally). See doi:10.1136/practneurol-2016-001584 *Fasciculations are involuntary muscle twitches localised to small areas of a muscle.  What is a stroke? Ischaemic Intracerebral Subarachnoid Hemorrhage Hemorrhage 80% 15% 5% Stroke, also known as cerebrovascular accident (CVA), is when impaired blood flow to the brain results in cell death. Stroke is characterised by acute onset and persistence of neurologic signs and symptoms beyond 24 hours. Ischaemic stroke often caused by thrombus is the most common type of stroke (accounts for about 80% of cases). A transient ischaemic attack (TIA) is caused by a temporary cut in blood supply to the brain, due to the partial blockage of an artery. While it is sometimes called a mini stroke, a TIA does not usually cause long-term brain damage. A TIA has identical symptoms to a stroke, but these last for less than 24 hours and are followed by a full recovery. A TIA is a powerful warning that an area of the brain is being deprived of blood and that a stroke may follow in the next few hours, days, weeks or months. Urgent medical attention is needed. ACE Check their FACE. Has their mouth drooped? RMS Can they lift both ARMS? PEECH Is their SPEECH slurred? Do they understand you? IME is critical. If you see any of these signs, call 000 now! Stroke incidence in Australia 60,000 new cases each year Death 475,000 25% survivors within a within a Disability month year 65% 20% 33% new stroke every 9 minutes National Stroke Foundation, 2017  Risk factors Diabetes Mellitus: 2 – 5 Excess alcohol consumption times greater risk Carotid atherosclerosis Age: >60 yrs risk of stroke doubles with every decade Hypercoagulable states Gender: male Some oral contraceptive pills Hypertension Atrial fibrillation Cigarette smoking Endocarditis Drug abuse, such as Obesity cocaine or amphetamine Hyperlipidemia Lack of exercise  Ischemic stroke http://www.uwmedicine.org/uwmed/Templates/content/uwmedicine  Mechanisms of Ischemic stroke Neuropathology Cerebral embolism Thrombus from elsewhere breaks off to lodge in brain blood vessels. Most often in the middle cerebral artery (MCA). Abrupt onset. Lysis of embolus may lodge fragments in distal branches and thus change symptoms. Possible secondary hemorrhage. Kandel, Principles of Neural Science  Mechanisms of Ischemic Neuropathology stroke Lacunar stroke Small (< 1.5cm) lesions caused by occlusions in deep branches of large vessels to subcortical structures (often in diabetes and hypertension). Often cause pure motor or pure sensory symptoms. Brainstem, internal capsule, basal ganglia, thalamus lesions are common, also multiple lesion sites are possible. More rapid and greater neurological recovery. http://www.uwmedicine.org/uwmed/Templates/content/uwmedicine  MechanismsHaemorrhagic of Neuropathology stroke Cerebral haemorrhage Common cause is rupture of aneurysm. Usually in deep branches of large vessels to subcortical structures (thalamus and putamen, 10% cerebellum). Neurological symptoms progress over time as haematoma and edema continues to increase. Very high mortality and severity of symptoms, but also more profound neurological recovery (as edema resolves and pressure is released). http://www.uwmedicine.org/uwmed/Templates/content/uwmedicine  MechanismsHaemorrhagic of Neuropathology stroke Subarachnoid haemorrhage (SAH) Common cause rupture of arterial aneurysm leading to bleeding into subarachnoid space. Aneurysmal SAH can cause cerebral vasospasm which appears several days after bleeding. This is because irritating blood byproducts cause the walls of an artery to contract. The cerebral vasospasm can produce ischemic neurological deficit identical to that produced by other causes of stroke. Up to 50% patients will re-bleed in 6 months. http://www.uwmedicine.org/uwmed/Templates/content/uwmedicine  Terminology Definitions Ataxia inability to coordinate muscle activity during voluntary actions – jerky movements. Often due to disorders of the cerebellum or the posterior spinal columns. May involve limbs, head, or trunk. Apraxia is characterized by loss of the ability to execute or carry out familiar movements, despite having the desire and physical ability. Aphasia impairment of language, affecting the production or comprehension of speech and the ability to read or write. Agnosia (a-gnosis, "non-knowledge", or loss of knowledge) is a loss of ability to recognize objects, persons, sounds, shapes or smells while the specific sense is not defective nor is there any significant memory loss.  Terminology Definitions Dyskinesia means "abnormal movement“; uncontrollable, often jerky movements that a person does not intend to make. Hemiparesis weakness on one side of the body. Person can still move the affected side of your body, but with reduced muscular strength. Dysphagia difficulty in swallowing due to problems in nerve or muscle control. Compromises nutrition and hydration and may lead to aspiration pneumonia & dehydration. Hemineglect or neglect syndrome inability of a person to process and perceive stimuli on one side of the body or environment, where that inability is not due to a lack of sensation. The effect of the location of lesion Cerebral vascular territories Anterior cerebral artery Middle cerebral artery Posterior cerebral artery The effect of the location of lesion Cerebral vascular territories MCA – Middle cerebral artery Kandel Schwartz & Jessel ACA – Anterior cerebral (2000).artery Principles of Neural PCA – Posterior cerebral Scienceartery 4/e McGraw-Hill.  Middle cerebral artery stroke Contralateral hemiparesis more pronounced in arm and face with leg less influenced. Gaze deviation away from the side of weakness towards the side of the cortical damage. Examples of symptoms which are hemisphere specific: Left (dominant) hemisphere aphasia (language disorders) some apraxias (including verbal) Right (non-dominant) hemisphere neglect syndrome Kandel Schwartz & Jessel (2000). Principles of Neural dressing apraxia Science 4/e McGraw-Hill.  Neglect (right hemisphere) The drawings on the right were made by patients with unilateral visual neglect following lesion of the right posterior parietal cortex. Kandel Principles of Neural Science 4/e  Anterior cerebral artery stroke Reduction of the function of the portions of the brain supplied by ACR: the medial aspects of the frontal and parietal lobes, basal ganglia, anterior fornix and anterior corpus callosum. Typical functional consequences: paralysis or weakness of the contralateral foot and leg, sensory loss in the contralateral foot and leg, gait apraxia, impairment of gait and stance, anosmia – problems with smell.  Posterior cerebral artery stroke Reduction of the function of the portions of the brain supplied by PCA: occipital lobe, a large portion of the thalamus, and the upper brainstem and midbrain. Mostly sensory dysfunction Symptoms related to visual system dysfunction and processing. Contralateral homonymous hemianopsia or hemianopia (loss of half of the visual field on the same side in both eyes). Kandel Schwartz & Jessel (2000). Principles of Neural Science 4/e McGraw-Hill.  Basilar artery stroke Patients with acute basilar artery occlusion have a mortality rate of greater than 85%. Sudden death/loss of consciousness. Proximal and mid portions of the basilar artery (pons) can result in patients being 'locked in' (patient is aware but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body, sometimes only eye movements are present). Somnolence, hallucinations and dreamlike behaviour. Coma, apnoea, cardiovascular instability. Kandel Schwartz & Jessel (2000). Principles of Neural Science 4/e McGraw-Hill.  Recovery after stroke Neurological deficits resulting from a stroke are often referred to as impairments. Functional deficits are often referred to as disabilities. Neurological recovery is defined as recovery of neurological impairments and is often the result of brain recovery/reorganization; it has been increasingly recognized as being influenced by rehabilitation.  Recovery after stroke Intrinsic neurological recovery and spontaneous reorganisation after stroke Peak spontaneous neurological recovery from stroke occurs within the first 1-3 months. This includes cortical reorganisation, cell function recovery but also adjusting the gain of spinal reflex loops to adapt to decreased descending input. At the spinal level the state of areflexia and muscle weakness that immediately follows a stroke is gradually replaced by the recovery of neuronal and network excitability, leading to improvements in residual motor function, but also increasing risk of developing spasticity. Spontaneous reorganisation after stroke may introduce maladaptive changes, especially if motor commands result in no movement and thus no proprioceptive feedback which would be able to uphold existing neural circuits and protect them from maladaptive plasticity.  Recovery after stroke Prominent recovery occurs during the first 3-6 months after the stroke and depends on rehabilitation procedures which promote brain plasticity and are required to establish new functional circuits replacing the damaged ones. A number of studies have shown that recovery may continue at a slower pace for at least 6 months. Some of the recovery is due to brain’s healing process, however, rehabilitation is crucial for promoting and shaping brain’s circuits during reorganisation period. This type of recovery and rehabilitation is critically time dependent! If rehabilitation is too late, there will be no effect as spontaneous healing/reorganisation processes will be finished and maladaptive changes may take place. In later stages the efficiency of rehabilitation relies on different plasticity mechanisms, which have no time limit.  Recovery after stroke Functional or adaptive recovery Functional recovery is defined as improvement in mobility and activities of daily living; it is significantly driven by rehabilitation. Function could be regained by learning compensatory movements. Functional recovery is influenced by neurological recovery but is not dependent on it. This recovery depends on the patient's motivation, ability to learn and family support as well as the quality and intensity of therapy.  Rehabilitation for stroke To relearn lost function damaged nervous system needs the same things that a normal nervous system needs to learn command signals, feedback about outcomes, intact brain regions to compare intended and actual movements. Many promising techniques that follow this principle proprioceptive stimulation of paretic or paralyzed limb, constraint induced therapy, augmented feedback systems, EMG assisted FES (functional electrical stimulation).  Rehabilitation for stroke Wii-hab