Spontaneous recovery post ischaemic stroke refers to mechanisms of neural recovery occurring intrinsically within the brain. The amount of recovery seen in the initial few weeks and months post event is reliant upon several neural mechanisms and processes.
“The first 2 to 3 months after stroke are crucial for spontaneous neuroplasticity, which refers to the natural course of neurophysiological repair and cortical reorganisation.”
An acute ischaemic cerebral event is a dynamic process with damage to brain tissue evolving over a short period of time. Initial insult due to lack of blood flow results in two identifiable areas of damage: core and penumbra. The core is the area of ‘direct hit’ resulting in tissue death and is considered non-salvageable. Surrounding the core is brain tissue (of collateral damage) which is at significant risk of being incorporated into the core of dead tissue. Generally, the larger the core the larger the extent of impairment, disability and a poorer outcome.
Neurological recovery is attributed to resolving oedema, the return of blood circulation to the penumbra, and diaschisis reversal. These local central nervous system (CNS) processes occur early on in neural recovery. Cortical reorganisation occurs later in recovery and is particularly influenced by active rehabilitation therapies and treatment.
- Sudden occlusion of a cerebral blood vessel causes oxygen and glucose depletion to brain cells. A cascade of pathological changes is triggered almost immediately leading to cellular damage and death.
- Elevated blood pressure (BP) may help in perfusing the salvageable penumbra. Caution is recommended by researchers in treating and lowering BP in the acute stage of stroke management. “An adverse effect of BP-lowering has been observed in a recent case series in which fifty nine per cent of the patients received antihypertensive medication within twenty four hours of stroke onset.”
- Recanalisation of the brain’s vasculature via thrombolysis therapy promotes reperfusion. There is a small window of opportunity for this treatment to be effective and safe. A risk for cerebral haemorrhage is realised in six per cent of cases.
“Thrombolysis and clot retrieval are medical interventions aimed at penumbra salvage. Currently only 15% of ischaemic strokes receive thrombolysis due to a therapeutically ‘short window of opportunity’. Clot retrieval in Australia is provided in large tertiary hospital settings with relatively few cases being performed at this point.”
- The swelling of the neurons and glia cells due to acute hypoxia (cytotoxic oedema) occurs initially post ischaemic insult, and followed later by vasogenic oedema.
“During an ischaemic stroke, a lack of oxygen and glucose leads to a breakdown of the sodium-calcium pumps on brain cell membranes, which in turn results in a massive buildup of sodium and calcium intracellularly. This causes a rapid uptake of water and subsequent swelling of the cells”
- Close monitoring of conscious state, blood glucose levels (BGL) and oxygen saturations in the first few days post ischaemic event is recommended. The goal of care is euglycaemia and oxygen saturations greater than ninety five per cent with or without supplemental oxygen. A decrease in Glasgow Coma Scale score greater than two could be indicative of development of moderate to severe cerebral oedema or haemorrhagic transformation requiring quick intervention.
- Diaschisis is a state of depressed activity (neural shock) due to the loss of input from the damaged area of the brain in an anatomically separate but neurally interconnected area of the brain.
- As blood flow improves and the inflammation and oedema resolves, diaschisis begins a reversal process with the affected area becoming more active and functional.
From a purely neurobiological level, this may be thought of as the only true level of recovery in the strictest sense of the word, in that the same brain circuits are facilitating function post injury as they were pre injury.
The National Stroke Foundation (NSF) Stroke Guidelines 2010 provide clinicians with recommendations and evidence to support clinical decision making. Efforts in the first few days and weeks post event is aimed at:
- Enriching the cerebral environment for penumbra salvage and minimising the core size and resultant damage; and
- Implementation of treatments, therapies and strategies to optimise known neural recovery mechanisms.
Clinicians working with stroke patients must know and understand the evidence and research behind the clinical guidelines and recommendations for stroke management.
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- Grefkes, C & Fink, GR 2011, ‘Reorganisation of cerebral networks after stroke: new insights from neuroimaging with connectivity approaches’, Brain: A Journal of Neurology, vol. 134, pt. 5, pp. 1264-76, doi:10.1093/brain/awr033.
- Lakhan, SE, Kirchgessner, A & Hofer, M 2009, ‘Inflammatory mechanisms in ischemic stroke: therapeutic approaches’, Journal of Translational Medicine, vol. 7, pp. 97, doi: 10.1186/1479-5876-7-97.
- Mattle, HP, Kappeler, L, Arnold, M, Fischer, U, Nedeltchev, K, Remonda, L, Jakob, SM & Schroth, G 2005, ‘Blood Pressure and Vessel Recanalization in the First Hours After Ischemic Stroke’, Stroke, vol. 36, no. 2, pp. 264-269, doi:10.1161/01.STR0000153052.59113.89.
- Moskowitz, MA, Lo Eng, H & Ladecola, C 2010, ‘The Science of Stroke: Mechanisms in Search of Treatments’, Neuron, vol. 67, no. 7, pp. 181-198, doi:10.1016/J.Neuron.2010.07.002.
- National Stroke Guidelines 2010, Clinical Guidelines for Stroke Management, no. ISSBNO-978-0-9805933-3-4, Melbourne, Australia.
- Nudo, RJ 2011, ‘Neural bases of recovery after brain injury’, Journal of Communication Disorders, vol. 44(S), pp. 515-520, doi: 10.1016/j.jcomdis.2011.04.004.
- Sharma, VK, Teoh, HL, Wong, LYH, Su, J, Ong, BK & Chan, BPL 2010, ‘Recanalization Therapies in Acute Ischemic Stroke: Pharmacological Agents, Devices, and Combinations’, Stroke Research and Treatment, doi:10.4061/2010/672064.