Key Clinical Concepts

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Pierce Parrish
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Cerebrovascular Review and General Vascular Syndromes, Including Those That Impact Dizziness Key Clinical Concepts Basic Review of Cerebrovascular Circulation Circulation to the brain is divided into

1 Cerebrovascular Review and General Vascular Syndromes, Including Those That Impact Dizziness Key Clinical Concepts Basic Review of Cerebrovascular Circulation Circulation to the brain is divided into anterior and posterior divisions. The anterior division is made up of the internal carotid arteries, the anterior cerebral arteries, the anterior communicating artery, and the middle cerebral arteries. The arteries of the anterior division supply the anterior regions of the brain, such as the frontal lobes, the parietal lobes, and the superior regions of the temporal lobe. The posterior division is made of vertebral arteries that have a branch called the posterior inferior cerebellar artery (PICA) and then unite to from one basilar artery. The basilar artery then has branches off of it that include the anterior inferior cerebellar artery (AIC) and pontine branches. The basilar artery then divides back into two arteries, which are the posterior communicating arteries. The posterior communication arteries then have a branch called the posterior communicating artery, which connects with the internal carotid artery. The connection of the posterior communicating arteries with the internal carotid artery

2 and the branches of the anterior cerebral arteries with the internal capsule form a round vascular structure called the Circle of Willis.

3 Cerebrovascular Collateral Shunting to Support Brain Therapy Understanding cerebral vasculature can also help a clinician design rehabilitation protocols. Once a clinician understands the specific functions in regions of the brain and their associated vasculature, they can design therapies that engages shunting of blood to that region to encourage recovery. For example, if an individual suffers from Broca s dysphagia, the clinical can use frontal eye field exercises such as saccades to activate the branches of the middle cerebral artery to shunt blood to those specific regions. The clinician can also be supportive in rehabilitation despite activating regions of the brain with different neurological functions. Mechanisms of Cerebrovascular Insults Several mechanisms of pathology occur involving the cerebral arteries, including ischemic stroke, hemorrhagic stroke, lacunar stroke, transient ischemic attack (TIA), microvascular disease, and migraine. Stroke or cerebrovascular accident (CVA) occurs when occluded blood flow leads to neuron death. There are two main types of CVA: Hemorrhagic stroke and ischemic stroke. Approximately 90 percent of strokes are ischemic. With hemorrhagic stoke the artery ruptures leading to vascular compromise. With ischemic stroke, either an emboli or a thrombus blocks vascular circulation of an artery. A clot that occurs in the artery and then travels down to a narrow division of the artery leading to occlusion is called a thrombus. A clot that breaks off or an obstructive source that breaks free and travels around into the cerebral vasculature to finally get stuck in a smaller artery is called an embolus. Many different types of substances can become an embolus, such as a blood clot, cholesterol from an atherosclerotic plaque, fat droplets from a bone fracture, air emboli from a gas bubble, septic emboli from bacteria containing pus, tissue emboli from small fragments of tissue, and foreign body emboli. A lacunar stroke is a small (0.2-15m in diameter) infarct caused by the occlusion of a single penetrating branch of a larger blood vessel that provides blood to the brain s deep structures, such as the basal ganglia. It usually does not involve the outer cortical regions of the brain. Lacunar infarcts typical occur in the basal ganglia, lenticular nuclei, and especially the putamen, thalamus, and white matter of the internal capsule, and pons. Lacunar infarcts occasionally occur in the cerebellum, cerebral gyri, and spinal cord.

4 There are five classic lacunar syndromes: Pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, and clumsy- hand dysarthria. The most common type is a pure motor hemiparesis, which accounts for percent of lacunar syndromes. These occur from infarction in the corona radiate, internal capsule (especially the genu and posterior limb), pons, or medullary pyramid. This leads to pure motor hemiparesis, such as paralysis of the face, arm, and leg on one side without visual field defects, dysphasia, or sensory deficits. It should be noted that cortical infarction rarely causes pure motor hemiparesis. A pure sensory stroke occurs in 6 7 percent of lacunar syndromes. These usually occur in the corona radiate of the posterior limb of the internal capsule and in the thalamus. The symptoms in a pure sensory type of lacunar syndrome are limited to persistent or transient numbness and mild sensory loss over one side of the body, including the face, arm, and leg, without associated hemiparesis, visual field defect, brainstem dysfunction, memory loss, dyslexia, or other deficits. The patient typically complains of paresthesia such as numb, hot, asleep, itching, dead, or heavy sensations with the associated body regions. A sensorimotor stroke includes a motor and sensory deficit as the name implies and occur in about 20 percent of cases. They usually occur in the posteroventral thalamus or in the internal capsule. Ataxic hemiparesis occurs in approximately 18 percent of lacunar infarctions and is named because of a combination of weakness and incoordination. It presents with weakness of the lower limb, especially the ankle and toes, and positive Babinski signs associated with dysmetria of the arm and leg on the same side. These are caused by lesions that simultaneously interrupt pyramidal systems (weakness) and adjoining frontopontocerebellar systems (ataxia) in the upper basis pontis. Dysarthria- Clumsy Hand Syndrome occurs in 2 16 percent of lacunar strokes with clinical presentations of facial weakness, severe dysarthria, dysphagia, and mild hand weakness and clumsiness. These lacunar infarcts can occur in the upper paramedian base of the pons or in the internal capsule. Outside of the five classic lacunar syndromes many lacunar infarcts occur in the basal ganglia, leading to hemichorea, hemiballsim, dystonia, restless leg syndrome, etc.

5 A transient ischemic attack (TIA) is a transient episode of neurological dysfunction caused by ischemia (loss of blood flow) without significant death (infarction) of neurons. However, neuron injury can still occur in TIA lasting only a few minutes. Additionally, having a TIA is a risk factor for eventually having a stroke. Symptoms of a TIA resolve in 24 hours or less. TIA causes identical presentation of stroke with accompanying hemiparesis, dysarthria, sudden numbness, mental confusion, etc. Symptoms can vary widely but the most frequent symptoms include temporary loss of vision, difficulty speaking (aphasia), hemiparesis, and paresthesia. The most common cause of a TIA is an embolus that occludes an artery in the brain, usually from an atherosclerotic plaque in one of the carotid arteries. Cerebral microvascular disease, or cerebral small vessel disease, includes white matter lesions and lacunar infarcts associated with ongoing cognitive, motor, gait, and mood disturbances. They are caused by loss of integrity of the arterial blood vessel microstructure. They are typically found in the elderly and can lead to dementia and parkinsonism. Hypertension is the most common predisposing factor. Migraines are a neurovascular disorder with evidence supporting its mechanisms start with the brain and then spread to the blood vessel. In other words, their mechanism appears to be due to dysautonomia. Risk factors include stress, hormone imbalances, brain injury, etc. About percent of people with migraines experience migraine with aura that precedes the headaches. Auras appear gradually over a number of minutes and generally last less than 60 minutes. Symptoms can be visual, sensory, or motor. Visual disturbances such a scintillating scotoma (an area of partial alteration in the filed of vision that flickers and may interfere with a person s ability to read or drive) are the most common followed by sensory aura that usually presents with feelings of pins- and- needles that begin in one side in the hand and arm and then spread to the nose and mouth area on one side. Motor symptoms in aura are not as common but can include hemiplegic migraine. Risk Factors for Cerebrovascular Pathology There are many risk factors for stroke, but basically it involves mechanisms that impact the integrity of blood vessels. Oxidative stress injures blood vessels. Factors that increase free radicals and increase risk for cerebral artery pathology include smoking, glycosylated end products from diabetes, systemic inflammation, and metabolic diseases such as hypothyroidism, metabolic syndrome, testosterone deficiency in men, estrogen deficiency in women, etc. We also know that infections

6 such as H. Pylori can circulate in the vascular system and induce injury to blood vessels. Injury to blood vessels over time can lead to hemorrhagic stroke or the development of atherosclerosis plaque, increasing risk for thromboembolic ischemic stroke. Vasculature Insults that Can Induce Dizziness and Vertigo Vascular mechanisms that can induce vertigo include vestibular migraine, vertebrobasilar insufficiency, and vascular infarctions. Vestibular migraine is a migraine that is directly caused by migraine and often associated with the diagnosis of basilar- type migraine. The clinical presentation of vestibular migraine with spontaneous or positional vertigo. Some experience a sequence of spontaneous vertigo that transforms into positional vertigo later in the attack. The duration and frequency of the attacks can vary between patents. Vestibular migraines can range from seconds (about 10%) and minutes (30%) to hours (30%) and up to several days (30%). For some patients it may take weeks to recover from an attack. Vertigo usually precedes headache as associated with an aura or the vertigo may occur late in the headache phase. Also, many patients experience both attacks with and without headache in prodrome. Vertigo and headache never occur together. Photophobia, phonophobia, osmophobia, and visual or other auras commonly accompanies vestibular migraine. Precipitants of the attacks may serve as diagnostic clues such as menstruation, sleep deficiency, stress, specific foods (cheeses, wines, MSG), intense lights, etc. The general neurological, vestibular, and ontological exam in vestibular migraine is normal. In addition to migraines, vascular infarcts involving the cerebellum or blood supply to the vestibular apparatus and vertebrobasilar insufficiency can cause vertigo. Vascular syndromes that can cause vertigo include lateral medullary syndrome (posterior inferior cerebellar artery, lateral pontine syndrome (anterior inferior cerebellar artery), labyrinthine artery syndrome, superior cerebellar artery syndromes, and vertebrobasilar insufficiency. Brainstem infarctions of the the brainstem and cerebellum can cause acute symptoms of vertigo that typically occur abruptly and usually last several minutes and transient isolated vertigo is the common manifestation of vertebrobasilar insufficiency. Lateral Medullary Syndrome, (or Wallenberg syndrome) is an acute ischemic infarct due to occlusion of the vessels supplying the lateral medulla oblongata; most commonly occlusion of intracranial portion of the vertebral artery followed by PICA and its branches. This syndrome is characterized by vestibulocerebellar symptoms: vertigo, falling towards the side of lesion, diplopia, and multidirectional nystagmus (inferior cerebellar peduncle and vestibular nucleus). Autonomic dysfunction: ipsilateral Horners s, hiccups. Sensory symptoms:

7 initially abnormal stabbing pain over the ipsilateral face then loss of pain and temperature sensation over the contralateral side of body (spinal trigeminal nucleus involvement) ipsilateral bulbar muscle weakness: hoarseness, dysphonia, dysphagia, and dysarthria, decreased gag reflex (nuclear ambiguous). Lateral Pontine Syndrome results from occlusion of AICA is considered rare, but generally results in lateral pontine syndrome, also known as AICA syndrome. The symptoms include sudden onset of vertigo and vomiting, nystagmus, dysarthria, falling to the side of the lesion (due to damage to vestibular nuclei), and a variety of ipsilateral features including hemiataxia, loss of all modalities of sensation of the face (due to damage to the principal sensory trigeminal nucleus), facial paralysis (due to damage to the facial nuclei), and hearing loss and tinnitus (due to damage to the cochlear nuclei). Patients with infarction in the territory of the AICA may have isolated recurrent vertigo, fluctuating hearing loss, and/or tinnitus as the initial symptoms 1-10 days prior to the infarction due to vertebrobasilar insufficiency that progresses to stroke. Labyrinthine Artery Syndrome occurs with compromise of internal auditory artery (IAA). The IAA is a branch of AICA and irrigates the cochlea and vestibular labyrinth. IAA infarction mostly occurs due to thrombotic narrowing of the AICA itself or the basilar artery at the orifice of the AICA. This leads to combined loss of vestibular and auditory function. Superior Cerebellar Artery Syndrome leads to symptoms are ipsilateral ataxia, nausea and vomiting, slurred (pseudobulbar) speech, loss of pain and temperature over the opposite side of the body. Partial deafness, tremor of the upper extremity, an ipsilateral Horner syndrome. Clinically, this stroke may be impossible to distinguish from a partial AICA or PICA territory stroke. It is much rarer than either one. Vertebrobasilar Insufficiency (VBI) refers to a condition in which blood flow to the vertebral and basilar arteries is restricted, thereby providing transient insufficient blood flow to the posterior portions of the brain. While VBI may be the result of a congenital abnormality, it is more commonly the result of atherosclerosis and resultant narrowing of the blood vessels. The characteristics of atherosclerotic plaque at the vertebral artery origin are unique from the morphological and pathological nature of plaque associated with the carotid. The symptoms due to VBI vary according to which portions of the brain s posterior circulation experience significantly decreased blood flow. Symptoms of VBI include loss of vision in one or both eyes, double vision, dizziness (vertigo), numbness or tingling in the hands or feet, nausea and vomiting, slurred speech, changes in mental status including confusion, drop attacks, loss of balance and coordination, and difficulty swallowing.

Stroke School for Internists Part 1

Stroke School for Internists Part 1 November 4, 2017 Dr. Albert Jin Dr. Gurpreet Jaswal Disclosures I receive a stipend for my role as Medical Director of the Stroke Network of SEO I have no commercial