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 initial two to three months after the event is a crucial period for spontaneous neuroplasticity, the 'naturally-occurring course of neurophysiological repair and cortical reorganisation of language functions'. (Robertson and Fitzpatrick, cited in Shah et al. 2013).

Penumbra Salvaging

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 and 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.

Reperfusion

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.
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.

Damaged brain tissue during an ischaemic stroke.

Oedema Management

The swelling of the neurons and glia cells due to acute hypoxia (cytotoxic oedema) occurs initially post-ischaemic insult, and is followed later by vasogenic oedema.
Close monitoring of conscious state, blood glucose level (BGL) and oxygen saturation in the first few days post-ischaemic event is recommended. The goal of care is to achieve euglycaemia and oxygen saturations of greater than 95% with or without supplemental oxygen. A decrease in the Glasgow Coma Scale score more than two could be indicative of development of moderate to severe cerebral oedema or haemorrhagic transformation requiring quick intervention.

Diaschisis Reversal

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 are 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.

(NSF 2010)

Clinicians working with stroke patients must know and understand the evidence and research behind the clinical guidelines and recommendations for stroke management.

References

Engelhardt, E & da Mota Games, M 2012, ‘Shock, Diaschisis and von Monakow’, Arquivos de Neuro-Psiquiatria, vol. 71 no. 7, pp. 487-489, https://www.scielo.br/scielo.php?script=sci_arttext&pid=S0004-282X2013000700487
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, https://pubmed.ncbi.nlm.nih.gov/21414995/
Lakhan, SE, Kirchgessner, A & Hofer, M 2009, ‘Inflammatory Mechanisms in Ischemic Stroke: Therapeutic Approaches’, Journal of Translational Medicine, vol. 7 pp. 97, https://translational-medicine.biomedcentral.com/articles/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, https://pubmed.ncbi.nlm.nih.gov/15637309/
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, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2957363/
National Stroke Foundation 2010, Clinical Guidelines for Stroke Management, NSF, https://www.pedro.org.au/wp-content/uploads/CPG_stroke.pdf
Nudo, RJ 2011, ‘Neural Bases of Recovery After Brain Injury’, Journal of Communication Disorders, vol. 44(S), pp. 515-520, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3162095/
Shah, P P, Szaflarski, J P, Allendorfer, J & Hamilton, R H 2013, ‘Induction of Neuroplasticity and Recovery in Post-stroke Aphasia by Non-invasive Brain Stimulation’, Front Hum Neurosci., vol. 7, viewed 13 October 2020, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3870921/
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, https://www.hindawi.com/journals/srt/2010/672064/

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