Now, let's talk a bit about brainstem stroke syndromes. The most common brainstem stroke syndromes is Wallenberg syndrome, when the posterior inferior cerebellar artery is affected. Less common brainstem stroke syndromes include the anterior inferior cerebellar arterial stroke syndrome, the medial medullary syndrome, basilar artery thrombosis, Weber syndrome, Benedict syndrome, and Millard-Gubler syndrome. In the posterior inferior cerebellar arterial syndrome, otherwise known as Wallenberg syndrome or lateral medullary syndrome, patients afflicted with this can have vertigo, they can have ipsilateral hemiataxia, dysarthria, dysphagia, ptosis, meiosis, contralateral body loss of pain and temperature, and ipsilateral facial loss of pain and temperature. In anterior inferior cerebellar arterial syndrome, they can have vertigo, ipsilateral deafness, ipsilateral facial weakness, and ataxia. In medial medullary syndrome, they can have contralateral hemiparesis sparing the face, hemicentric loss of posterior column type contralaterally, tongue weakness ipsilateral to the site of the infarct, upbeat nystagmus, and involvement of the 11th cranial nerve or spinal accessory nerve. In basilar artery thrombosis, this is often referred to as Lochtan syndrome, where you essentially are functionally tetrapyretic or tetraplegic, but your cognition is intact so you can think and you also have ocular motor function. So patients often with basilar artery thrombosis, they can communicate by ocular movement with a yes-no system. In Weber syndrome, which involves a stroke involving the base of the midbrain in the brainstem that involves the cranial nerve three involving ocular motor palsy with crossed hemiplegia. In Benedict syndrome, involving the tectum of the midbrain, it involves, again, cranial nerve number three with ocular palsy, gaze paralysis, and cerebellar ataxia. Millard-Gubler syndrome, this is when a stroke involves the base of the pons in the brainstem, and this can involve cranial nerves six and seven with contralateral hemiparesis. Question. What is the most typical pattern of motor recovery in patients after a left middle cerebral arterial distribution stroke? A. Initial hypertonia, then hypotonia. B. Recovery from distal to proximal. C. Synergy followed by voluntary control. D. Greatest recovery six months later. The answer is C. Synergy followed by voluntary control. The usual recovery is voluntary control preceded by non-functional synergistic muscle contraction pattern, initial hypotonia followed by hypertonia, recovery of motor function in a proximal to distal fashion, and most of the motor recovery takes place within the first six months. Hemorrhagic stroke. The most common cause of hemorrhagic stroke is hypertension, and the most common areas affected by hemorrhagic stroke include the basal ganglia, thalamus, pons, and cerebellum. There are also causes of hemorrhagic stroke not due to hypertension. These can include an arterial venous malformation, a brain aneurysm, amyloid angiopathy, especially in the elderly, and a tumor where it can bleed into a tumor causing a hemorrhage. What's the role of brain imaging in hemorrhagic stroke? In the acute phase to identify the process and its degree of severity, subsequently approximately four to six weeks post-acute phase to rule out underlying processes such as tumor, arterial venous malformation, or an abscess, and the physiatrist has an important role to ensure that this brain imaging occurs either by the physiatrist or by the neurologist or neurosurgeon caring for the patient. Learning objective number three, describe an appropriate stroke etiologic workup for a patient who has been admitted to your inpatient rehabilitation unit in order to be sure that it has been completed sufficiently. Diagnostic and etiologic evaluation of stroke includes laboratory, lipid profile, and hypercoagulable panel, EKG, to rule out atrial fibrillation and left ventricular hypertrophy. Fortunately, most of the time the laboratory and EKG have been performed before coming to an inpatient rehabilitation unit, but what has been occurring on greater frequency is implantable cardiac monitoring for months or longer versus an external cardiac monitoring for up to 30 days to rule out arrhythmias. Also, echocardiography, whether it's transthoracic or transesophageal, usually occurs before the patient comes to acute inpatient rehabilitation or subacute inpatient rehabilitation, as is the case generally with carotid artery duplexes and brain imaging, including diffusion and perfusion-weighted images. Magnetomography or CT scans. These are fast, and this is usually important in an emergency setting, and they're relatively inexpensive. CT scans can help confirm the diagnosis of stroke and other intracranial processes. From the 2018 American Heart Association and American Stroke Association update, in most cases CT scans will provide the necessary information to make management decisions. Sometimes patients cannot undergo magnetic resonance imaging, so they must have CT scans, such as if they have cardiac pacemakers, implantable cardiac defibrillators, some spinal hardware, and some joint arthroplasties. Magnetic resonance imaging includes diffusion-weighted imaging, or DWI, which is sensitive in diagnosing ischemic stroke. One can also do both diffusion-weighted imaging and perfusion-weighted imaging, or PWI, which may help to demonstrate the existence and size, if present, of the ischemic penumbra, an area that may be salvageable in the early stage. Carotid ultrasound or carotid duplex. This is a noninvasive assessment of the carotid arterial patency. It can identify the presence or absence of carotid arterial stenosis. Cardiothoracic surgeons will generally obtain an additional study, such as a traditional angiogram or more likely a CT or an MR angiogram, for further anatomic information if the carotid duplex reveals what appears to be significant stenosis. Transcranial Doppler also has a role to get a sense of the direction and velocity of blood flow within the circle of Willis, and it can detect vasospasm in intracranial collateral pathways. Traditional angiography can be done for these patients, but magnetic resonance angiography, while not as sensitive as traditional angiography, is being done with greater frequency, and this can determine the presence of arterial venous malformations, aneurysms, angiitis, and arterial dissections, and to determine the presence of carotid arterial stenosis, and if so, how severe it is. Echocardiography, transthoracic or TTE, can assess the heart valves and estimate the left ventricular ejection fraction. Transesophageal echocardiography, or TEE, can assess the atria of the heart, cea clot, heart valves, aorta, pulmonary artery, atrial septum, and coronary arteries, and can assess left ventricular ejection fraction more accurately than a transthoracic echocardiography, and can also detect the presence of a patent foramen ovale, or PFO. Lumbar puncture, or LP, can detect blood in the cerebral spinal fluid that may be helpful in diagnosing a subarachnoid hemorrhage if and when head CT is negative. Lumbar puncture has a very limited role in ischemic stroke. Which type of magnetic resonance imaging technique is the most sensitive for assessing acute brain ischemia? A. Proton gradient imaging B. MRI with magnetic resonance angiography C. Diffusion-weighted imaging D. Spin echo imaging The answer is C, diffusion-weighted imaging. Diffusion-weighted magnetic resonance imaging is the most sensitive MRI type for assessing acute ischemic stroke, and is used in stroke centers to guide therapeutic decisions. Immediate medical management of stroke includes the ABCs, airway, breathing, circulation, blood pressure control, intravenous access, intravenous hydration, and in the acute stages generally NPO or nothing by mouth. Treatment of hypertension in acute stroke is critical. In acute ischemic stroke, for a patient who has not received tissue plasminogen activator or TPA, lowering blood pressure may be potentially harmful. If the patient is eligible for a tissue plasminogen activator or TPA, you may want to treat the blood pressure if the systolic blood pressure is greater than 185 mmHg or the diastolic blood pressure is greater than 110 mmHg. You may use intravenous libidolol, nicardipine, or clevidipine. You may also use intravenous enalaprilat or sodium nitroprussides, and as soon as possible to try to wean off intravenous agents and switch to oral agents. In intracerebral hemorrhage or hemorrhagic stroke, lowering blood pressure is usually helpful because increased blood pressure can increase the size of the hemorrhagic stroke. So in general, you try to target blood pressure systolically less than 160 mmHg. That can be done in various ways by using intravenous libidolol, nicardipine, clevidipine, enalaprilat, or sodium nitroprusside, and again, similarly to acute ischemic stroke, you would want to wean off these intravenous agents as soon as possible and transition to oral agents. Seizure management can be life-threatening and can increase intracranial pressure. For severe seizures, a first-line treatment can be a short-acting intravenous benzodiazepine. Otherwise, oral long-acting agents such as levitteracetam valproic acid or divalprox can also be used. Regarding intracranial pressure management, you want to keep this under 20 mmHg by correcting underlying factors such as hypoxia, hyperthermia, acidosis, hypotension, hypovolemia, and hypercarbia. You may want to elevate the head of bed at 30 degrees, hyperventilate the patient. Medications can be used such as mannitol, furosemide, or barbiturates, fluid restriction, and if necessary, neurosurgical decompression. This is a slide that reveals the ischemic penumbra, which is an area of the brain that is potentially salvageable by interventional factors. So it is key to understand that time equals brain.

brainstem stroke syndromes

Wallenberg syndrome

motor recovery after left middle cerebral arterial distribution stroke

hemorrhagic stroke causes

stroke etiologic workup