The brain stem consists of the midbrain, pons, and medulla. Brain stem infarction commonly occurs due to an embolus occluding large arteries (vertebral or basilar arteries) supplying it or due to an embolus traveling from the heart, or atherosclerotic plaques from the large arteries (vertebral, basilar) [1]. Brainstem infarcts are relatively less common as compared to hemispheric infarcts [2]. The common clinical presentation is sudden onset focal neurological deficits like hemiparesis, vertigo, orthostatic symptoms, diplopia, and lower cranial nerve paralysis with dysphagia, and hoarseness. Vertigo is the cardinal feature of brain stem infarction [2] followed by ipsilateral cranial nerve symptoms, contralateral hemiplegia, hemianesthesia (crossed motor or sensory signs) with bilateral involvement of the sensory tract or motor tract or both.

A few uncommon clinical features of brain stem infarction include "salt and pepper" facial pain [3], blepharospasm [4], palatal myoclonus [2], hiccough [5], tinnitus in medullary infarction [6], bruxism and trismus in basilar artery occlusion [7], and peduncular hallucinosis in midbrain infarction [8]. If there is total occlusion of the vertebrobasilar system then patients can present with tachycardia, fluctuating blood pressure, ataxia, impaired consciousness, and coma leading to death. Pontine or midbrain infarction can also present as "locked-in syndrome" in which the affected individual has sudden onset vomiting, transient loss of consciousness with quadriplegia, bilateral facial palsy, anarthria (total loss of articulation), and bilateral oculomotor nerve palsy resulting in loss of voluntary eye movements [2].

Clinical features specific to the ischemic involvement of the different regions of the brainstem are:

Midbrain: ipsilateral oculomotor (3rd cranial nerve) paralysis with contralateral hemiplegia (Weber syndrome)

Pons: 5th, 6th, 7th and 8th cranial nerve involvement, diplopia, dysarthria, vertigo, gait abnormality, and/or sensation of ear canal block, sustained horizontal nystagmus, conjugate eye movements when the gaze is directed towards the side of hemiparesis [6], ataxic hemiparesis.

Medulla: 9th, 10th, 11th and 12th cranial nerve involvement, pure motor hemiparesis if the medullary pyramid is the site of the infarction; sensory motor hemiplegia if the medial lemniscus is involved; or Dejerine syndrome wherein there is ipsilateral tongue paralysis with contralateral hemiplegia. A patient presenting with acute onset vertigo and then developing sudden respiratory failure is likely to have a medullary infarct.

The aim of the workup is to determine the characteristics of the vascular lesion and the etiology of the brain stem infarction. A detailed history during workup provides clues to the risk factors and etiology of the condition while a thorough neurological, cardiovascular, and bedside glucose testing are mandatory to determine further workup and management.

Computed tomography scanning (CT) is performed first to differentiate between an ischemic infarct and hemorrhagic stroke as it has 95% sensitivity in identifying hemorrhage especially if done within 24 hours of onset of symptoms [9] [10]. Occluded and dolichoectatic arteries can be identified better with spiral CT angiography [11] [12]. Magnetic resonance imaging (MRI) has greater sensitivity than CT in the identification of ischemia with small lacunar infarcts being seen only on MRI. Diffusion-weighted MRI is highly sensitive for early ischemia and should be ordered after the CT scan. MRI and magnetic resonance angiography (MRA) are useful in detecting dissection, demyelinating plaques, vertebrobasilar dolichoectasia, and dissection. [13] [14] [15].

In addition, other tests are indicated based on the clinical evaluation to detect the etiology and risk factors of the brainstem infarct:

Cardiac factors: electrocardiography (in all cases), telemetry or holter monitoring, serum troponin (in cases suspected to have myocardial ischemia), and echocardiography [16] especially in patients under 45 years of age or in those with basilar artery occlusion.

Vascular factors: blood tests to rule out thrombotic disorders (homocysteine levels, antiphospholipid antibodies, protein S, protein C, antithrombin III, factor V Leiden) and routine tests like complete blood count, platelet count, PT/PTT, fasting blood glucose, lipid profile, and serology for syphilis.

Autoimmune factors: antinuclear antibodies, rheumatoid factor, erythrocyte sedimentation rate.

Urine toxicology and drug screening for stimulants like cocaine and amphetamines.

The treatment of brain stem infarction focuses on restoring blood flow and minimizing damage. In the acute phase, medications such as thrombolytics may be used to dissolve blood clots. Antiplatelet drugs or anticoagulants can help prevent further clot formation. Supportive care, including respiratory support and management of blood pressure, is often necessary. Rehabilitation therapies, such as physical, occupational, and speech therapy, play a crucial role in recovery by helping patients regain lost functions.

The prognosis for brain stem infarction varies depending on the severity and location of the stroke, as well as the patient's overall health. Some individuals may recover fully, while others may experience long-term disabilities. Early intervention and rehabilitation can significantly improve outcomes. However, due to the critical functions controlled by the brain stem, some patients may face life-threatening complications or require long-term care.

Brain stem infarctions are primarily caused by the interruption of blood flow due to a clot or blockage in the arteries supplying the brain stem. Risk factors include high blood pressure, high cholesterol, smoking, diabetes, and a history of cardiovascular disease. In some cases, emboli (clots that travel from other parts of the body) can lodge in the brain stem's blood vessels, leading to an infarction.

Brain stem infarctions are less common than strokes affecting other parts of the brain, accounting for a small percentage of all strokes. They can occur in individuals of any age but are more prevalent in older adults due to the increased risk of vascular disease. Men are slightly more likely to experience brain stem strokes than women, and certain populations with higher rates of cardiovascular risk factors may be more susceptible.

The pathophysiology of brain stem infarction involves the disruption of blood supply to the brain stem, leading to ischemia (lack of oxygen) and subsequent cell death. The brain stem's dense network of neurons and its role in vital functions make it particularly vulnerable to damage. The specific effects depend on which areas of the brain stem are affected, as different regions control different functions.

Preventing brain stem infarctions involves managing risk factors and maintaining a healthy lifestyle. This includes controlling blood pressure, cholesterol, and blood sugar levels, as well as avoiding smoking and excessive alcohol consumption. Regular physical activity and a balanced diet can also reduce the risk. For individuals with a history of stroke or cardiovascular disease, medications such as antiplatelets or anticoagulants may be prescribed to prevent future events.

Brain stem infarction is a serious medical condition resulting from interrupted blood flow to the brain stem. It presents with a range of symptoms due to the brain stem's role in controlling vital functions. Diagnosis involves clinical evaluation and imaging, while treatment focuses on restoring blood flow and rehabilitation. The prognosis varies, with early intervention improving outcomes. Understanding the risk factors and pathophysiology is crucial for prevention and management.

If you or someone you know experiences sudden symptoms such as dizziness, difficulty speaking, or weakness on one side of the body, it is important to seek medical attention immediately. Brain stem infarctions require prompt diagnosis and treatment to minimize damage and improve recovery chances. Managing risk factors like high blood pressure and cholesterol can help prevent such events. Rehabilitation therapies are essential for regaining lost functions and improving quality of life after a stroke.

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