Stroke Recovery

 

Science  06 Apr 2018: Vol. 360, Issue 6384, pp. 30-31

Supporting recovery from brain injury

Simon Rumpel

Institute of Physiology, Focus Program Translational Neurosciences, University Medical Center of the Johannes Gutenberg University Mainz, Hanns-Dieter-Hüsch Weg 19 55128 Mainz, Germany.

[paraphrase]

As an organ with a disproportionally large energy consumption (∼20% of the total energy is used by the brain, which is only ∼2% of human body weight), normal brain function ceases within seconds after interruption of blood supply. Typically, a blood clot blocks the blood flow in the case of an ischemic stroke; less frequently, a blood vessel bursts, leading to hemorrhagic stroke. Within minutes,    neurons will be permanently damaged    and undergo cell death during the next hours, often involving a phase of neuronal hyperactivity. Apart from the neurons located within the core area immediately affected by trauma or loss of blood supply, additional loss of neurons is also observed in the surrounding brain areas, the so-called penumbra. Here, a temporarily decreased blood flow    and pathologically increased neuronal activity    spreading over from the core area    endangers neighboring neurons.

The size and location of the affected brain area varies substantially among individuals and therefore so does the degree of resulting functional impairment. A stroke, for example, is often recognized by the sudden development of deficits in the motor control of limbs and loss of control of facial muscles and speech production. The phase of acute injury to the brain lasts a few hours and, in a fraction of cases—typically involving large trauma or widespread hemorrhagic bleeding—can lead to the death of the patient.

The acute phase is immediately followed by a recovery phase that is characterized by a spontaneous lessening of behavioral impairments that can last for weeks to many months. During this recovery phase, cascades of molecular alterations are observed that reflect changes in gene expression, increased release of growth factors, and regrowth of neuronal processes. The recovery phase    transitions to the chronic stage, when the rate of functional improvements does not increase and in many cases leaves affected persons with lifelong impairments associated with considerable loss in quality of life.

What are the mechanisms that help the brain in many cases to spontaneously recover at least partially from functional impairments? The neurons of the brain make an estimated 10¹³ synaptic connections and thereby create a highly complex network.    A single neuron in the cortex, the outer shell of the brain, receives signals from a few thousand neurons and in turn sends out signals to a similarly large number of downstream neurons. Despite that, in the adult brain the number of neurons is largely constant, the connections among them are not hardwired. Brain circuits have the ability to undergo plastic remodeling    by building new and eliminating old synapses    as well as adapting the strength of persistent connections. This synaptic plasticity is believed to mediate cognitive processes such as the storage of information during memory formation in healthy conditions, but after brain injury, synaptic plasticity helps to reconfigure neuronal circuits and thus to regain functionality. An emerging picture from longitudinal imaging studies in animal models is that neuronal microcircuits display a substantial level of dynamic remodeling even under conditions that do not require behaviorally or pathologically induced adaptation and thus represents a fundamental property of the brain.

The molecular mechanisms underlying plastic changes of synapses have been under intense investigation for decades. A major finding was that the receptors for neurotransmitters at the synapse are not fixed but undergo continuous and tightly regulated turnover that allows fast increases or decreases in total receptor number and thus connection strength.

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