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Brainstem Infarction


Brainstem Infarction

Article Author:
Supreeth Gowda
Article Editor:
Orlando De Jesus
Updated:
7/10/2020 4:24:04 PM
For CME on this topic:
Brainstem Infarction CME
PubMed Link:
Brainstem Infarction

Introduction

The brainstem is composed of the midbrain, the pons, and the medulla oblongata, situated in the posterior part of the brain. It is a connection between the cerebrum, the cerebellum, and the spinal cord. Embryologically, it develops from the mesencephalon and part of the rhombencephalon, all of which originate from the neural ectoderm. The brainstem is organized internally in three laminae: tectum, tegmentum, and basis. Gray matter in the brainstem is found in clusters all along the brainstem to forming mostly the cranial nerve nuclei, the pontine nuclei, and the reticular formation. White matter in the form of various ascending and descending tracts can be found mainly in the basis lamina, which is the most anterior part.[1] The brainstem is responsible for multiple critical functions, including respiration, cardiac rhythm, blood pressure control, consciousness, and sleep-wake cycle. The cranial nerve nuclei that are present in the brainstem have a crucial role in vision, balance, hearing, swallowing, taste, speech, motor, and sensory supply to the face. The white matter of the brainstem carries most of the signals between the brain and the spinal cord and helps with its relay and processing. 

The blood supply to the brainstem is mostly from the vertebrobasilar system. The blood supply can be divided into a group of arteries supplying each region:[2]

  1. Midbrain:
    1. Anteromedial: supplied by the posterior cerebral artery. 
    2. Anterolateral: supplied by the posterior cerebral artery and branches of the anterior choroidal artery.
    3. Lateral: supplied by the posterior cerebellar artery, the choroidal artery, and the collicular artery. 
    4. Posterior: supplied by the superior cerebellar artery, the posteromedial choroidal artery.
  2. Pons:
    1. Anteromedial: supplied by the pontine perforating arteries, branches of the basilar artery. 
    2. Anterolateral: supplied by the anterior inferior cerebellar artery. 
    3. Lateral: supplied by the lateral pontine perforating arteries, branches of the basilar artery, anterior inferior cerebellar artery, or the superior cerebellar artery. 
  3. Medulla oblongata:
    1. Anteromedial: supplied by the anterior spinal artery and vertebral artery. 
    2. Anterolateral: supplied by the anterior spinal artery and vertebral artery. 
    3. Lateral: supplied by the posterior inferior cerebellar artery. 
    4. Posterior: supplied by the posterior spinal artery. 

Brainstem infarction is an area of tissue death resulting from a lack of oxygen supply to any part of the brainstem. The knowledge of anatomy, vascular supply, and physical examination can be life-saving in the setting of an acute infarct and provide precise diagnosis and management. Time becomes an essential factor in management. Early intervention has shown dramatically reduced morbidity and mortality.[3]

Etiology

Brainstem infarction refers to the sequelae of ischemia to any part of the brainstem, due to the loss of blood supply or bleeding. Occlusion and stenosis of the posterior circulation cause significant hypoperfusion in the brainstem. The most common etiologies for brainstem infarction are atherosclerosis, thromboembolism, lipohylanosis, tumor, arterial dissection, and trauma. In medulla oblongata infarcts, 73% are due to stenosis of the vertebral artery, 26% due to arterial dissection, and rest being caused by other causes like cardioembolic.[4] However, the number of infarcts due to cardioembolic etiology increase to 8% in pontine infarcts and 20% to 46% in midbrain infarcts.[5] 

Risk factors for stroke, in general, include hypertension, diabetes mellitus, metabolic syndromes, hyperlipidemia, tobacco use, obesity, history of ischemic heart disease, atrial fibrillation, sleep apnea, lack of physical activity, use of oral contraceptives, fibromuscular dysplasia, trauma, and spinal manipulation.[2][6][7]

Epidemiology

Globally, there is a rise in lifestyle diseases like cardiovascular disease, stroke, diabetes mellitus, both in developed and developing nations. The global burden of stroke can be measured at 122 million disease-adjusted life years.[8] In the US, a stroke is reported every 40 seconds.[9] It has been estimated that the brainstem accounts for 10% to 15% of all strokes.[6] The lifetime (age 25 and onwards) risk of stroke in males is between 23.3 to 26.0%, and in females is between 23.7% to 26.5%. There is variation between regions with Eastern Sub-Saharan Africa with the lowest lifetime risk of 11.8% to East Asia, with the highest risk of 38.8%. China has the most significant lifetime estimated risk of 39.3%.[10]

Pathophysiology

The pathophysiology of all infarcts is the lack of oxygen in the tissue, leading to its death. The human brain requires 20% of oxygen consumption even though it accounts for only 2% of the body by weight.[11] The cerebral blood flow is autoregulated to maintain a constant level of perfusion and adequate venous drainage to deal with all its needs. The cerebrum is also unique as it has little to no energy stores and uses glucose as its primary energy source, with distally produced ketone bodies being used only in starvation.[12] Dependence on aerobic respiration and low respiratory reserve makes the brain susceptible to ischemia and eventually causing irreversible tissue death. The cellular cascade of events is as follows:[13] 

  • Depletion of ATP due to lack of aerobic respiration in the mitochondria.
  • Loss of function of membrane ion pumps and impaired voltage gradient across membranes, leading to cellular edema.
  • Excitotoxicity of the neurons due to the release of glutamate and synaptosomal-associated protein 25, causing further deterioration of energy levels and membrane ion potentials. Production of reactive oxygen species and free radicals, leading to cell death.

While the above apoptotic/ necrotic pathway is in process, specific protective pathways are triggered: 

  • Expression of heat shock protein 70, B-cell lymphoma 2 gene family, and prion protein to prevent activation of the apoptotic cascade.
  • Release of Neurotrophin-3, interleukin-10, and granulocyte-colony stimulating factor, helping in the activation of survival pathways and reduction of proinflammatory cytokine activities.

The cellular cascade is potentially reversible, which can lead to vasogenic edema over the next few hours. Vasogenic edema causes an increase in pressure in the surrounding tissue, leading to mass effect, and worsening the situation.[14] The eventual release of matrix metalloproteinases causes loss of structural integrity and the dissolution of the blood-brain-barrier.[15]

In the case of hemorrhagic etiology, the rupture of blood vessels causes hypoxia, pressure effects, and chemical irritation of brain tissue due to the disruption of blood-brain-barrier.

History and Physical

A loss of about 1.9 million neurons in the brain happens each minute in an untreated stroke.[16] Hence a targeted approach must be followed with clear objectives. Assessment of airway, breathing and circulation, and its stabilization as a patient with brainstem stroke can present with trauma, altered mental status, altered respiratory drive, hypoxia, vomiting, and or mechanical airway obstruction.

Establishing the time of ischemic insult is critical. Patients, family members, attenders, co-workers, first responders, or any reliable witness can determine the time the patient was last known normal. If in the case of deficits arising in one's sleep, last known normal is the time the patient went to bed. A clinician needs to distinguish between ischemia and its differential diagnosis, causing various neurological deficits. Reliable information about the patient's current medication, especially with regards to oral hypoglycemic, insulin, anti-epileptics, neurological or psychological drugs, anti-platelets or blood thinners, drug abuse or overdose, and sleep apnea must be established. Co-morbidities and risk factors need to be assessed. Evaluation of signs and symptoms for hemorrhagic stroke is life-saving. Any history of uncontrolled hypertension, sudden onset of headache, vomiting, signs of raised intracranial pressure must raise high suspicion of hemorrhage and warrants an immediate non-contrast computed tomographic (CT) scan of the head.

Brainstem lesions can be divided into three broad categories to identify the affected region or function of the brainstem.[2][17]

  • Ascending and descending pathways: Weakness, loss of pain and temperature sensation, ataxia, Horner syndrome, loss of position and vibration sensation, gaze palsy
  • Nuclei and cranial nerves: Ocular and extraocular muscle weakness, loss of sensation over the face, autonomic dysregulation, dysphagia, dysarthria, dysphonia, vertigo, alteration in taste and hearing
  • Integrative and other functions: Choreoathetosis, tremors, ataxia, central dysautonomia, gaze paresis, lethargy, locked-in syndrome 

A concise physical examination should evaluate any signs suggestive of trauma, meningeal irritation, or neurological deficits. Neurological examination of a brainstem infarct must include the following assessment:

  • Levels of consciousness and higher mental function
  • Complete evaluation of cranial nerves and its functions
  • Motor and sensory system examination, including reflexes, neglect, speech, and language
  • Cerebellar signs, coordination, and gait
  • Autonomic system

Evaluation

The initial evaluation of patients presenting with a suspected stroke of the brainstem includes vital signs, oxygen saturation, blood pressure, pulse rate, respiratory rate, fingerstick blood glucose levels, non-contrast CT scan of the head or brain magnetic resonance imaging (MRI). Non-contrast CT scan of the head is a quick and widely available imaging modality, and it is highly sensitive for acute hemorrhage. On a head CT scan, blood can be seen as a hyper-dense lesion. Infarction of brain tissue can be detected by brain MRI diffusion-weighted images and fluid-attenuated inversion recovery images, which are highly sensitive in the hyper-acute setting.[18]

Blood workup should including complete blood count, coagulation profile, serum electrolytes, renal function, lipid panel, hemoglobin-A1c level, thyroid function, vitamin B12 level, and vitamin D levels. Other blood investigation for hypercoagulability states, autoimmune conditions, liver pathologies, and genetic tests can be obtained. Cardiovascular workup for atrial fibrillation with either an electrocardiogram or Holter monitor, echocardiogram, cardiac enzyme levels, chest X-ray should be obtained. A multi-phase CT angiography can establish the state of vertebral and carotid arteries, along with assessment for any endovascular management. Sleep study or polysomnography is diagnostic for various sleep disorders and must be suspected in stroke cases with unknown etiologies. Evaluation of both modifiable and non-modifiable risk factors for cardiovascular disease must be done.

Due to the high density of nuclei and fibers running through the brainstem, the lesion in various structures gives rise to different signs and symptoms. Variously named stroke and stroke syndromes have been described in the literature.

  • The 'top-of-the-basilar' syndrome:[19] Also known as the rostral brainstem infarction. It results in alternating disorientation, hypersomnolence, unresponsiveness, hallucination, and behavioral abnormalities along with visual, oculomotor deficits, and cortical blindness. Occurs due to occlusion of the distal basilar artery and its perforators.
  • Ondine's syndrome:[19] Affects the brainstem response centers for automatic breathing. It results in complete breathing failure during sleep but normal ventilation when awake. The blood supply affected is the pontine perforating arteries, branches of the basilar artery, anterior inferior cerebellar artery, or the superior cerebellar artery.
  • One-and-a-half syndrome:[20] Affects the paramedian pontine reticular formation and medial longitudinal fasciculus. It results in the ipsilateral conjugate gaze palsy and internuclear ophthalmoplegia. The blood supply affected is the pontine perforating arteries and branches of the basilar artery.  

Midbrain syndromes[21][22][23][24]

  • Claude syndrome: Affects the fibers from CN III, the rubrodentate fibers, corticospinal tract fibers, and corticobulbar fibers. It results in ipsilateral CN III palsy, contralateral hemiplegia of lower facial muscles, tongue, shoulder, upper and lower limb along with contralateral ataxia. The blood supply involved is from the posterior cerebral artery.
  • Dorsal midbrain syndrome (Benedikt): Also known as paramedian midbrain syndrome, affects the fibers from CN III and the red nucleus. It results in ipsilateral CN III palsy, contralateral choreoathetosis, tremor, and ataxia. The blood supply involved comes from the posterior cerebral artery and paramedian branches of the basilar artery.
  • Nothnagel syndrome: Affects the fibers from CN III and the superior cerebellar peduncle. It results in ipsilateral CN III palsy and ipsilateral limb ataxia. It can be due to quadrigeminal neoplasms and is often bilateral.
  • Ventral midbrain syndrome (Weber): Affects the fibers from CN III, cerebral peduncle (corticospinal and corticobulbar tract), and substantia nigra. It results in ipsilateral CN III palsy, contralateral hemiplegia of lower facial muscles, tongue, shoulder, upper and lower limb. The involvement of substantial nigra is present can result in a contralateral movement disorder. The blood supply affected is the paramedian branches of the posterior cerebral artery.

Pontine syndromes[23][25][26][27][28][29][30]

  • Brissaud-Sicard syndrome: Affects the CN VII nucleus and corticospinal tract. It results in ipsilateral facial cramps and contralateral upper and lower limb hemiparesis. The blood supply affected is the posterior circulation. Rarely, the syndrome can arise due to brainstem glioma.
  • Facial colliculus syndrome: Affects the CN VI nucleus, the CN VII nucleus, and fibers and the medial longitudinal fasciculus. It results in lower motor neuron CN VII palsy, diplopia, and horizontal conjugate. It can occur due to neoplasm, multiple sclerosis, or viral infection.
  • Gasperini syndrome: Affects the nuclei of CN V, VI, VII, VIII, and the spinothalamic tract. It results in ipsilateral facial sensory loss, ipsilateral impaired eye abduction, ipsilateral impaired eye abduction, ipsilateral nystagmus, vertigo, and contralateral hemi-sensory impairment. The blood supply involved derives from the pontine branches of the basilar artery and long circumferential artery of the anterior inferior cerebellar artery.
  • Gellé syndrome: Affects the CN VII, VIII, and corticospinal tract. It results in ipsilateral facial palsy, ipsilateral hearing loss, and contralateral hemiparesis.
  • Grenet syndrome: Affects CN V lemniscus, CN VII fibers, and spinothalamic tract. It results in altered sensation in the ipsilateral face, contralateral upper, and contralateral lower limbs. It can arise due to neoplasm. 
  • Inferior medial pontine syndrome (Foville syndrome): Also known as the lower dorsal pontine syndrome, affects corticospinal tract, medial lemniscus, middle cerebellar peduncle, and the nucleus of CN VI and VII. It results in contralateral hemiparesis, contralateral loss of proprioception & vibration, ipsilateral ataxia, ipsilateral facial palsy, lateral gaze paralysis, and diplopia. The blood supply affected is from branches of the basilar artery.
  • Lateral pontine syndrome (Marie-Foix syndrome): Affects the nuclei of CN VII, & VIII, corticospinal tract, spinothalamic tract, and cerebellar tracts. It results in contralateral hemiparesis, contralateral loss of proprioception & vibration, ipsilateral limb ataxia, ipsilateral facial palsy, lateral hearing loss, vertigo, and nystagmus. The blood supply affected is the perforating branches of the basilar artery and the anterior inferior cerebellar artery.
  • Locked-in syndrome: Affects upper ventral pons, including corticospinal tract, corticobulbar tract, and CN VI nuclei. It results in quadriplegia, bilateral facial palsy, and horizontal eye palsy. The patient can move the eyes vertically, blink, and has an intact consciousness. The blood supply affected is the middle and proximal segments of the basilar artery.
  • Raymond syndrome: Affects the CN VI fibers, corticospinal tract, and corticofacial fibers. It results in an ipsilateral lateral gaze palsy, contralateral hemiparesis, and facial palsy. The blood supply involved is from the branches of the basilar artery.
  • Upper dorsal pontine syndrome (Raymond-Cestan): Affects the longitudinal medial fasciculus, medial lemniscus, spinothalamic tract, CN V fibers and nuclei, superior and middle cerebellar peduncle. It results in ipsilateral ataxia, coarse intension tremors, sensory loss in the face, weakness of mastication, contralateral loss of all sensory modalities. The blood supply involved is from the circumferential branches of the basilar artery.
  • Ventral pontine syndrome (Millard-Gubler): Affects the CN VI & VII and corticospinal tract. It results in ipsilateral lateral rectus palsy, diplopia, ipsilateral facial palsy, and contralateral hemiparesis of upper and lower limbs. The blood supply involved derives from the branches from the basilar artery.

Medulla oblongata[31][32][33][34][35]

  • Avellis syndrome: Affects the pyramidal tract and nucleus ambiguus. It results in ipsilateral palatopharyngeal palsy, contralateral hemiparesis, and contralateral hemi-sensory impairment. The blood supply affected is the vertebral arteries. 
  • Babinski-Nageotte syndrome: Also known as the Wallenberg with hemiparesis, affects the spinal fiber and nucleus of CN V, nucleus ambiguus, lateral spinothalamic tract, sympathetic fibers, afferent spinocerebellar tracts, and corticospinal tract. It results in ipsilateral facial loss of pain & temperature, ipsilateral palsy of the soft palate, larynx &  pharynx, ipsilateral Horner syndrome, ipsilateral cerebellar hemi-ataxia, contralateral hemiparesis, and contralateral loss of body pain and temperature. The blood supply involved is from the intracranial portion of the vertebral artery and branches from the posterior inferior cerebellar artery.
  • Cestan-Chenais syndrome: It affects the spinal fiber and nucleus of CN V, nucleus ambiguus, lateral spinothalamic tract, sympathetic fibers, and corticospinal tract. It results in ipsilateral facial loss of pain and temperature, ipsilateral palsy of the soft palate, larynx & pharynx, ipsilateral Horner's syndrome, contralateral hemiparesis, contralateral loss of body pain & temperature, and contralateral tactile hypesthesia. The blood supply affected is the intracranial portion of the vertebral artery and branches from the posterior inferior cerebellar artery.
  • Hemimedullary syndrome (Reinhold syndrome): Affects the nucleus & fiber of CN V, CN XII nucleus ambiguus, lateral spinothalamic tract, sympathetic fibers, afferent spinocerebellar tracts, corticospinal tract, and medial lemniscus. It results in ipsilateral Horner's syndrome, ipsilateral facial loss of pain & temperature, ipsilateral palsy of soft palate, larynx & pharynx, ipsilateral tongue weakness, ipsilateral cerebellar hemi-ataxia, contralateral hemiparesis, and contralateral face sparing hemihypesthesia. The blood supply involved is from the ipsilateral vertebral artery, the posterior inferior cerebellar artery, and branches from the anterior spinal artery. 
  • Jackson syndrome: Affects CN XII and pyramidal tract. It results in ipsilateral palsy of the tongue and contralateral hemiparesis. The blood supply involved is from the branches from the anterior spinal artery.
  • Lateral medullary syndrome (Wallenberg syndrome): Affects the spinal nucleus & fiber of CN V, nucleus ambiguus, lateral spinothalamic tract, sympathetic fibers, inferior cerebellar peduncle, and vestibular nuclei. It results in ipsilateral Horner's syndrome, ipsilateral facial loss of pain & temperature, ipsilateral palsy of soft palate, larynx & pharynx, ipsilateral cerebellar hemi-ataxia, contralateral loss of body pain & temperature, nystagmus, dysarthria, dysphagia, and hyperacusis. The blood supply affected is the vertebral artery and branches from the posterior inferior cerebellar artery.
  • Medial medullary syndrome (Dejerine syndrome): Affects the fibers of CN XII, corticospinal tract, and medial lemniscus spinal. Results in ipsilateral tongue weakness, ipsilateral loss of proprioception & vibration, contralateral hemiparesis, and contralateral face sparing hemihypesthesia. The blood supply affected is the branches from the vertebral artery and the anterior spinal artery.
  • Schmidt syndrome: Affects the fibers and nuclei of CN IX, X, XI, and pyramidal system. It results in ipsilateral palsy of the vocal cords, soft palate, trapezius, & sternocleidomastoid muscle, and contralateral spastic hemiparesis. The blood supply involved involves branches from the vertebral artery, the posterior inferior cerebellar artery the anterior spinal artery.
  • Spiller syndrome: Affects the fibers and nucleus of CN XII, corticospinal tract, and medial lemniscus spinal along with medial hemi-medulla. Results in ipsilateral tongue weakness, ipsilateral loss of proprioception & vibration, contralateral hemiparesis, and contralateral face sparing hemihypesthesia. The blood supply involved is from the branches from the vertebral artery and the anterior spinal artery.
  • Tapia syndrome: Affects the nucleus ambiguus, CN XII, and pyramidal tract. It results in ipsilateral palsy of the trapezius, sternocleidomastoid muscle, & half of the tongue, dysphagia, dysphonia, and contralateral spasmodic hemiparesis. The blood supply involved is from the branches from the vertebral artery, the posterior inferior cerebellar artery the anterior spinal artery.
  • Vernet syndrome: Affects the CN IX, X, and XI. It occurs due to compression in the jugular foramen

Treatment / Management

After the patient's airway, breathing and circulation have been stabilized, a timeframe of the patient's symptoms is obtained. Vitals and fluid status must be stabilized. Hypo or hyperglycemia must be corrected. Fever, if present, should be managed accordingly. Blood pressure must not be aggressively controlled to allow permissive hypertension only in the case of ischemic injury. Patients with last known normal within 4.5 hours can be considered as candidates for thrombolysis, whereas a 24 hour last known normal can be candidates for mechanical thrombectomy. If it is a case presenting earlier than 4.5 hours of onset, thrombolysis with intravenous recombinant tissue plasminogen activator significantly improves the clinical outcome.[36]

Tissue plasminogen activator (tPA)

Inclusion criteria for tPA:[36][37]

  • Clinical diagnosis of ischemic stroke
  • <4.5 hours of the onset of symptoms
  • Age >18 and <80 years
  • Symptoms of stroke presenting for more than 30 minutes

Excision criteria for tPA:[37][38]

  • Unknown timeline of onset of patient symptoms
  • Intracranial hemorrhage or any active bleeding
  • Persistently elevated blood pressure ≥ 185 mmHg systolic and ≥ 110 mmHg diastolic
  • Low platelets <100,000/mm3, altered INR >1.7, PT >15 sec or aPTT >40sec
  • Current use of anti-coagulant
  • Severe hypoglycemia <50mg/dL
  • History of previous intracranial hemorrhage
  • History of gastrointestinal bleeding in the past 21 days
  • History of intracranial or intraspinal surgery in the past 90 days
  • History of intra-axial intracranial neoplasm or gastrointestinal malignancy

Intravenous alteplase (recombinant tissue plasminogen activator) should be given at the dose of 0.9 mg/kg (maximum dose of 90 mg/kg) with 10% as the loading dose in the first minute. The patient must be under continuous observation. Anti-platelet therapy must be withheld for at least 24 hours post thrombolysis and restarted after a head CT scan without evidence of bleeding.

Mechanical endovascular thrombectomy in patients with large anterior circulation occlusion is well documented; however, most strokes affecting the brainstem arises from posterior circulation perforating branches. For those cases where the occlusion is at the main vertebral or basilar artery, endovascular thrombectomy is recommended for successful revascularization and favorable outcome.[39][40][41][42][43][44][45][46] Other studies have shown no evidence of a difference in favorable outcomes between endovascular therapy when compared to standard medical therapy alone.[47][48]

Antiplatelet therapy: The usage of acetylsalicylic acid as monotherapy or dual therapy along with clopidogrel within 24 – 48 hours after the onset of symptoms significantly improved patient outcomes.[49]

Management of risk factors like hypertension, diabetes mellitus, dyslipidemia, atrial fibrillation, thyroid abnormalities, sleep apnea, malignancies, and hypercoagulable states should be treated accordingly.  Dietary and lifestyle modification must be explained and discussed. Supplementation with vitamin B12 and vitamin D3 should also be considered. Physiotherapy, along with speech therapy, can be used if physical deficits arise due to infarct. Treatments must start at the earliest and must be aggressively pursued as the brain losses its plasticity within 90 days.

Differential Diagnosis

The differential diagnosis of brainstem infarction includes the following:

  • Transient ischemic attack
  • Metastatic disease of the brain

  • Central pontine demyelination

  • Subarachnoid hemorrhage

  • Seizures
  • Basilar migraine

  • Basilar meningitis

  • Cerebellopontine angle tumors

  • Supratentorial hemispheric mass effect with herniation and brainstem compression

  • Hypoglycemia

  • Electrolyte imbalance

  • Conversion disorder

Prognosis

Stroke is the primary cause of disability and a leading cause of mortality worldwide. Stroke has a burden of 122 million disease-adjusted life years, with gradual increasing incidences.[8] Early diagnosis and management have a lower chance of permanent morbidity. Untreated acute basilar artery occlusion has extremely high mortality approaching 90%. For those patients who receive adequate treatment, the one-year survival rate is between 60 to 80%.

The risk of stroke recurrence is 10 to 15%; hence regular follow up is advised. Early initiation of rehabilitative care is also recommended. Patients with significant neurological deficits have a worse prognosis. The final prognosis depends on various factors including, age, the severity of the stroke, etiology of stroke, location, structures involved, associated risk factors, co-morbidities, and the management.

Complications

  • Hemorrhagic transformation
  • Seizures
  • Aspiration pneumonia
  • Myocardial infarction, arrhythmias, and heart failure
  • Dysphagia and dysphonia
  • Depression and anxiety
  • Blackouts and falls
  • Sleep disorders
  • Urinary tract infection
  • Deep vein thrombosis
  • Pulmonary embolism
  • Dehydration and malnutrition
  • Pressure sores and skin lesions
  • Orthopedic complications and contractures
  • Post-stroke fatigue

Deterrence and Patient Education

ACT FAST is an acronym suggested by the American Stroke Association to recognize the early symptoms of a stroke. It has the following components:

  • F-Face drooping
  • A-Arm Weakness
  • S-Speech
  • T-Time to call 9-1-1

Along with the above symptoms, if the patient experiences any of the following, emergency medical services must be activated

  • Sudden confusion
  • Sudden trouble seeing
  • Sudden numbness
  • Sudden trouble walking
  • Sudden severe headache

Control of risk factors can significantly reduce future strokes:[50]

  • Smoking cessation
  • Alcohol use
  • Drug addiction and abuse
  • Hypertension and diabetes control
  • Obesity and sedentary lifestyle
  • Sleep apnea
  • Regular follow with primary care physician

Pearls and Other Issues

Here are some important considerations:

  • Early identification of stroke and its management: "Time is brain."
  • Avoiding pitfalls of stroke-like syndrome/episodes: Migraine headache, seizure disorder, transient ischemic attack, vertigo
  • Permissive hypertension to improve perfusion in ischemic stroke.
  • Patient education with "FAST" acronym

Enhancing Healthcare Team Outcomes

The diagnosis and management of brainstem stroke bring a considerable burden to the healthcare system, the patient, the family members, and the society at large. The slow increase in the global burden of stroke has been steadily increasing.

The enhancement must start with proper patient education about the risk factors and how they can be modified. A simple community educational approach about smoking cessation, a healthy diet, an active lifestyle, regular health screening for diabetes mellitus and hypertension, drug addiction cessation, and rehabilitation can be undertaken. A decentralized model where a community-level assessment of primary and secondary prevention of non-communicable disease can result in a reduction in the incidence of stroke.

Acute management of stroke in a peripheral setting must be managed with skilled individuals; however, a complete and robust interdisciplinary team of neurologists, physicians, psychiatrists, nurses, physiotherapists, and other paramedical staff is necessary for the best patient outcome. A trained first responder who can immediately stabilize the patient and prevent the deterioration is critical. Usage of the National Institutes of Health Stroke Scale or the Modified Rankin Scale or other standardized models and scales help clinicians with their decision.[51]

Constant root-cause analysis, frequent updates to local hospital protocol, and continued medical education should be implemented. The usage of telemedicine, teleradiology, and a rapid communication system can allow the various interprofessional to deploy rapidly and prevent long term complications. Examination of the patient must be done as a team, where each member can be delegated with certain aspects of evaluation and management. A multi-disciplinary approach has shown to prevent at least 80% of subsequent strokes.[50] [Level I, II]

Post-stroke rehabilitation care must include inputs from the clinicians, nurses, pharmacists, to obtain the best outcome for the patient. A healthy support system of dieticians and therapists, along with adequate domiciliary support, must be provided.



(Click Image to Enlarge)
Brainstem structures, deficits and vascular supply.
Brainstem structures, deficits and vascular supply.
Contributed by Supreeth Gowda N, MBBS

References

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