From the Guidelines
Focal neurological deficits require urgent evaluation and management, as they can be a sign of a life-threatening condition such as acute ischemic stroke, which may benefit from thrombolysis within a specific time window, as suggested by the most recent guidelines 1. When evaluating a patient with focal neurological deficits, a thorough neurological examination is essential, focusing on:
- Mental status
- Cranial nerves
- Motor function
- Sensory function
- Reflexes
- Coordination Urgent neuroimaging, typically with CT or MRI, is recommended to determine the underlying cause, which may include:
- Stroke
- Tumor
- Infection
- Trauma
- Demyelinating diseases The management depends on the specific cause; for instance:
- Acute stroke may require thrombolysis within a specific time window, as recent studies have shown the benefit of extending the thrombolytic window up to 9 hours using perfusion imaging 1
- Tumors might need surgical intervention The pattern and progression of focal deficits provide valuable diagnostic clues:
- Sudden onset suggests vascular causes like stroke
- Gradual progression might indicate a tumor or degenerative condition Prompt recognition and appropriate referral to neurological care are crucial for optimal outcomes, as delayed treatment can result in significant morbidity and mortality, as highlighted in the guidelines for stroke care 1.
From the Research
Definition and Diagnosis of Focal Neurological Deficits
- A focal neurological deficit is defined as the clinical expression of a structural or functional, transient or permanent abnormality that can be ascribed to a particular brain region 2
- Focal neurological deficits with sudden onset or rapid progression are alarming symptoms indicating a neurological disorder with often urgent need for treatment 3
Emergency Management of Focal Neurological Deficits
- The emergency management of focal neurological deficits may involve the use of EEG, particularly in cases of partial epileptic seizures or febrile context 2
- The use of tissue plasminogen activator (tPA) in the treatment of acute ischemic stroke may be associated with an increased risk of cerebral hemorrhage, but this risk can be reduced by combination therapy with mild hypothermia 4 or free radical spin trapping 5
Pathophysiology of Focal Neurological Deficits
- The tissue-type plasminogen activator-plasminogen activator inhibitor 1 complex may promote neurovascular injury in brain trauma by inducing matrix metalloproteinase-3 and increasing cerebrovascular permeability 6
- The formation of complexes between tissue plasminogen activator and plasminogen activator inhibitor-1 in the brain parenchyma may facilitate post-traumatic cerebrovascular damage 6