Brain attack: correlative anatomy.
Brain attack is a synonym for stroke. Brain attack or stroke is defined as a sudden neurologic deficit caused by interruption of blood flow to the brain.[1,4] This interruption of blood flow may be caused by cerebral thrombosis, embolism or hemorrhage.[1,4] The increasing use of the term brain attack by health care professionals is an attempt to convey the seriousness and urgency of stroke to the public.[1,2,3] Approximately 10% of brain attacks are preceded by transient ischemic attacks. Public education is being focused on prevention, recognition of symptoms and early treatment of brain attack.[1,2,3] Despite advances in the treatment of brain attack, it continues to be the third leading cause of death in the United States. Half of all patients hospitalized for acute neurological diseases are diagnosed with stroke, and stroke is the leading cause of long-term disability in the United States. Persons with brain attack are treated throughout the entire health care delivery system and require nursing care during the preventive and acute phase of illness on into the rehabilitative phases. Understanding brain anatomy as it relates to brain attack can provide the nurse with valuable knowledge. In addition to enhancing assessment skills and documentation, this knowledge can be used to plan nursing care. This article reviews basic cerebral arterial circulation and related brain anatomy, while correlating specific neurological deficits with the involved vessel and location of the brain attack.
Cerebral Arterial Circulation
The human brain has higher requirements for oxygen and glucose as compared to other organs. Approximately 20% of the resting cardiac output is supplied to the brain at a rate of 800-1000 ml of cerebral blood flow per minute.[8,23] Interruption of blood supply to the brain tissue for 2-5 minutes may result in permanent damage. Brainstem centers maintain blood pressure and cerebral perfusion.
Blood supply to the brain originates from the subclavian and the common carotid arteries. The common carotid artery bifurcates in the neck forming two branches: the internal carotid and the external carotid arteries. The external include arm apraxia and expressive aphasia. In distal occlusion of the anterior cerebral artery, the clinical, picture differs slightly with symptoms including contralateral upper and lower extremity weakness, contralateral sensory loss in the foot and motor and/or sensory aphasia.[4,8]
The middle cerebral artery (Figs 1, 2) also arises from the internal carotid artery. There are four branches of the middle cerebral artery. The main stem of the middle cerebral artery is the lenticuiostriate artery. This artery supplies blood to parts of the basal ganglia and fibers of the internal capsule.[4,8,12] Near the sylvian fissure, the middle cerebral artery separates into three cortical branches: the anterior temporal artery, superior trunk and inferior trunk.[4,8] These three vessels supply blood to the cortical surfaces of the parietal, temporal and frontal lobes. The pattern of middle cerebral artery occlusion determines which clinical symptoms a patient exhibits (Table 1). In complete occlusion symptoms include contralateral gaze palsy, hemiplegia, hemisensory loss, spatial neglect and homonymous hemianopia.[4,8] Global aphasia is present with left hemisphere lesions. Occlusion of the superior trunk of the middle cerebral artery will result in the following symptoms: contralateral hemiplegia and hemianesthesia in the face and arm with lesser involvement of the lower extremity, ipsilateral deviation of eyes and head, and Broca's aphasia (with dominant hemisphere occlusion).[4,8] Occlusion of the inferior trunk of the middle cerebral artery usually results in contralateral hemianopsia or upper quadrantanopia, Wernicke's aphasia (usually with left sided lesions) and left visual neglect (usually with right sided lesions). Motor or sensory deficits are usually absent.[4,8] Other occlusion patterns involving parts of the middle cerebral artery generally contain some degree of hemiplegia and aphasia with or without sensory loss.
Table 1. Correlation Between Anterior Blood Supply and Symptomatology in Brain Attack Artery Brain Structure Anterior choroidal Globus pallidus, lateral geniculate body, posterior limb of internal capsule, medial temporal lobe Ophthalmic Orbit and optic nerve Anterior cerebral Anterior three quarters of medial surface of cerebral hemispheres caudate nucleus, globus pallidus and the internal capsule Middle cerebral Cortical surfaces of the parietal, temporal and frontal lobes Basal ganglia and internal capsule Artery Signs/Symptoms of Occlusion Anterior choroidal Contralateral hemiplegia Hemihypesthesia Homonymous hemianopia Ophthalmic Transient mononuclear blindness or complete unilateral blindness Anterior cerebral Contralateral sensory and motor deficits greater in leg than arm Incontinence Deviation of the eyes and head toward the lesion Contralateral grasp reflex Abulic symptoms Arm apraxia Expressive aphasia (in dominant hemisphere occlusion) Motor and/or sensory aphasia (distal occlusion) Middle cerebral Complete: Spatial neglect and homonymous hemianopia Global aphasia (left lesion) Superior trunk: Contralateral hemiplegia and hemianesthesia in face and arm Ipsilateral deviation of eyes and head Broca's aphasia (usually left-sided) Inferior trunk: Contralateral hemianopsia or upper quadrantanopia Werknicke's aphasia (left lesion) Left visual neglect (right lesion)
[Figure 1-2 ILLUSTRATION OMITTED]
The posterior circulation (Table 2) is responsible for approximately only one fifth of the total cerebral blood flow. The posterior cerebral circulation is supplied by the subclavian arteries. The right subclavian artery is a branch of the innominate artery. On the left, the subclavian artery branches directly from the aorta. Each subclavian artery branches into a vertebral artery. Major branches of the vertebral arteries include: posterior spinal, anterior spinal and the posterior inferior cerebellar arteries (Fig 3). The anterior and posterior spinal arteries supply blood to the spinal cord. The posterior inferior cerebellar artery supplies blood to the medulla and the cerebellum.10 Symptoms associated with occlusion of the posterior inferior cerebellar artery vary and depend upon specific areas of brain injury. Infarction of the medial branch of the posterior inferior cerebellar artery produces vertigo, nystagmus, ataxia and persistent dizziness. When there is occlusion of the lateral branch of the posterior inferior cerebellar artery the clinical picture includes unilateral clumsiness with gait and limb ataxia. Often there is an inability to stand or a sudden fall. Vertigo, dysarthria and nystagmus or eye deviation may be present. When larger portions of the cerebellum and medulla are involved symptoms will be more extensive with changes in level of consciousness caused by increased intracranial pressure.
Table 2. Correlation Between Posterior Blood Supply and Symptomatology in Brain Attack Artery Brain Structure Vertebral Anterolateral parts of the medulla Posterior cerebral Occipital lobe, medial and inferior surface of temporal lobe, the midbrain, third and lateral ventricles Posterior inferior Medulla and cerebellum cerebellar Anterior inferior Cerebellum and pons cerebellar Superior cerebellar Upper part of cerebellum, midbrain Basilar Pons and midbrain Artery Signs/Symptoms of Occlusion Vertebral Contralateral impairment of pain and temperature sensation Posterior cerebral Contralateral hemiplegia, sensory loss and ipsilateral visual field deficits Posterior inferior Medial branch: cerebellar Vertigo, nystagmus, ataxia, persistent dizziness Lateral branch: Unilateral clumsiness with gait and limb ataxia Inability to stand Sudden falling Vertigo, dysarthria, occulomotor signs Anterior inferior Horner's syndrome, and contralateral cerebellar loss of pain and temperature sense of the arm, trunk and leg Superior cerebellar Slurred speech and contralateral loss of pain and thermal sensation Basilar Limb paralysis, bulbar or pseudobulbar paralysis of cranial nerve motor nuclei, nystagmus, coma or locked in syndrome
[Figure 3 ILLUSTRATION OMITTED]
Branches of the vertebral arteries supply the anterolateral parts of the medulla. Signs and symptoms of vertebral artery occlusion depend on location of blood supply interruption. In lateral medullary syndrome, clinical findings include contralateral impairment of pain and temperature sensation, ipsilateral Homer's syndrome, dysphagia, diminished gag reflex, vertigo, nystagmus and ataxia.[4,7]
The vertebral arteries join together at the medullopontine junction to form a single basilar artery (Fig 4). The basilar artery terminates at the junction of the pons and midbrain (Table 2). It is responsible for supplying blood to the pons and the midbrain.[8,10] Symptoms consistent with basilar artery occlusion include limb paralysis, bulbar or pseudobulbar paralysis of the cranial nerve motor nuclei, nystagmus, eye movement disturbances and coma.[4,8] Locked-in syndrome may occur with a complete occlusion of the basilar artery. Symptoms include consciousness with complete motor paralysis and the inability to communicate orally or by gesture.[4,8]
[Figure 4 ILLUSTRATION OMITTED]
Basilar artery branches include the posterior cerebral, posterior choroidal artery, anterior inferior cerebellar and superior cerebellar arteries.[10,12] The posterior cerebral artery supplies blood to the occipital lobes, medial and inferior surfaces of the temporal lobe, midbrain and third and lateral ventricles. When the posterior cerebral artery is occluded, the clinical symptoms include contralateral hemiplegia, sensory loss and ipsilateral visual field deficits.[6,23] The weakness seen with occlusion of the posterior cerebral artery is usually greater in the face and upper extremities.
The posterior choroidal artery penetrates the brain supplying the choroid plexus of the third ventricle and the dorsal surface of the thalamus. Infarct of this vessel has not been observed. The anterior inferior cerebellar artery is responsible for supplying blood to parts of the cerebellum and pons.[10,12] Clinical findings vary. These symptoms may include vertigo, nausea, vomiting, nystagmus, tinnitus, ipsilateral cerebellar ataxia and Homer's syndrome, contralateral loss of pain and temperature sense of the arm, trunk and leg.
The superior cerebellar artery (Table 2) supplies blood to the upper part of the cerebellum and the midbrain.[10,12] Brain attack of this vessel causes ipsilateral cerebellar ataxia, nausea, vomiting, slurred speech and contralateral loss of pain and thermal sensation.
The Circle of Willis (Fig 4) located at the base of the skull is a small area of less than one square inch. It is formed by branches of the internal carotid arteries and the vertebrobasilar system. These branches include the two anterior cerebral arteries, the anterior communicating artery, the two posterior communicating arteries and two posterior cerebral arteries. The anterior and meninges.[8,10] The external carotid artery can also serve as collateral circulation for an occluded internal carotid artery. The internal carotid artery continues through the neck and enters the skull before branching into the main arteries of the anterior cerebral circulation. The bilateral internal carotid arteries each supply two-fifths of the cerebral blood flow. The main branches of the internal carotid artery include: the ophthalmic artery, anterior choroidal artery, the posterior communicating artery, the anterior cerebral artery and the middle cerebral artery.
The ophthalmic artery (Table 1) supplies blood to the orbit and the optic nerve. Occlusion of the ophthalmic artery may result in transient mononuclear blindness or complete unilateral blindness. Transient mononuclear blindness or amaurosis fugax is characterized by a brief unilateral visual deficit lasting 15-30 minutes in length.[10,19] The multiple small branches of the ophthalmic artery connect with extensions of the external carotid circulation to provide a path for collateral circulation in cases of internal carotid occlusion.
The anterior choroidal artery (Table 1) is responsible for supplying blood to deep structures of the brain including the globus pallidus (basal ganglia), lateral geniculate body (thalamus), posterior limb of the internal capsule and medial temporal lobe.[8,17] Occlusion of the anterior choroidal artery results in contralateral hemiplegia, hemihypesthesia and homonymous hemianopia.
The anterior cerebral artery is a branch of the internal carotid artery (Fig 1). The anterior three quarters of the medial surface of the cerebral hemisphere, portions of the basal ganglia (caudate nucleus and globus pallidus) and the internal capsule are supplied by the anterior cerebral artery.[4,8.10] When there is occlusion of the entire anterior cerebral artery territory the clinical symptoms include contralateral sensory and motor deficits which are greater in the foot and leg than the arm (Table 1). Usually the face and hand are not involved.[4,8] In addition, clinical symptoms include incontinence, deviation of the eyes and head toward the lesion, contralateral grasp reflex and abulic symptoms.[4,8] These include apathy, decreased spontaneity and limited speech.[4,6,8] When the left anterior cerebral artery is occluded, additional symptoms may communicating artery connects the right and left internal carotid systems. The posterior communicating arteries allow for the connection of the anterior cerebral and posterior cerebral circulation.[8,10] In certain situations, the Circle of Willis maintains cerebral blood flow despite individual cerebral artery occlusion by permitting adequate blood supply to reach brain structures. Collateral cerebral circulation is dependent upon patency of the Circle of Willis vessels. Anomalous vessels may interfere with compensatory blood flow.[4,12] Collateral blood flow may also come from branches off the external carotid system.
Lobes of the Cerebrum
The frontal lobe is the largest lobe in the human brain, comprising almost 60% of the cerebrum. It's posterior margin lies on the fissure of Rolando (central fissure), thus dividing it from the parietal lobe. The inferior margin borders on the Sylvian fissure (lateral fissure) separating it from the temporal lobes.[18,23] The prefrontal region lies anterior to the motor area, located just anterior to the central fissure, while Broca's area is situated at the inferior frontal gyrus.
The prefrontal region provides added cortical space for cerebration to occur and assists the thalamus and hypothalamus with certain autonomic functions (respirations, gastrointestinal activity and blood pressure). It also facilitates concentration, abstract thought, memory, judgment, ethics, insight, emotion, tact and inhibition.[12,13,14] The prefrontal area sequences thoughts appropriately, evaluates consequences of actions and solves complicated intellectual functions. It guides behaviors in accordance within societal laws/morals and chooses behaviors that are appropriate to various situations.
The motor cortex is arranged somatotopically so that certain areas of this region control specific areas of the contralateral body. The giant Betz cells (pyramidal cells) control motor function of the various muscles spatially arranged on the strip. For example, muscle control for the feet is located in the area of the longitudinal fissure while facial control is located at the opposite end of the strip. The motor association area also provides connections for cranial nerves III, IV, VI, IX, X and XI.[12,18] Broca's area is primarily concerned with expressions of speech such as word formation and memory of motor patterns, depending on hemisphere dominance. Articulation, pronunciation, voice and speech production are all functions of this region of the frontal lobe.[12,14,23]
Deficits from a brain attack affecting the frontal lobe's anterior and middle cerebral arteries manifest a variety of symptoms. Memory, abstract thinking, judgment, ethical behavior, emotions, insight, tact and inhibition may all be altered in the individual. There may also be problems associated with turning of the eyes and head, trunk movement, flexion and extension of the extremities and coordinated eye movement. Nonfluent aphasia will often result with involvement of Broca's region. Words and syllables are uttered with effort because mouth, tongue and cheek motor functions are impaired. Comprehension of spoken language may be preserved; however, the individual may be apraxic and unable to correctly follow verbal cues even though he/she understands the meaning of the command.
The parietal lobe lies between the central sulcus and the parieto-occipital fissure. The lateral fissure divides the parietal and temporal lobes (Fig 3). Divisions of this lobe are the angular, supramarginal and postcentral gyri.
The primary function of the parietal lobe is to provide an interpretation of sensory input.[12,14] The primary somesthetic area is located in the postcentral gyrus which exercises sensory control over the opposite side of the body. The sensory cortex is arranged in the same type of topographical scheme as the motor strip with the feet being controlled by an area in the longitudinal fissure and facial muscles controlled by the temporal region.
Specific sensory qualities include two-point discrimination, pressure, weight, texture, body interpretation and orientation, pain, proprioceptive interpretation as well as deep bone and fascia sensations. The parietal lobe also recognizes the nature of complex objects by touch and form as well as the presence of one's own body.
Sensory deficits may occur with a brain attack. Unilateral neglect syndrome is common. If an individual reacts to what is perceived, he/she will attend to that specific perception. If an individual sees what is on the right side, he/she will only recognize the right side; consequently, left-sided neglect results. Other deficits in the parietal lobe could include paresthesias and/or diminished sensations for pain, touch, position sense and pressure.
The temporal lobe lies below the lateral fissure and posteriorly to the parieto-occipital fissure (Fig 3),[11,23] Primary auditory and associational areas are the major functional areas in this region.
The primary auditory area, also known as Wernicke's area, is located in the superior temporal gyrus. Its primary function is to receive and discriminate sounds. The secondary auditory area, which surrounds the primary area, is responsible for interpreting the sound. Also in this general area are olfactory tracts which originate in the inferior portion of the frontal lobe. They receive olfactory stimuli from cranial nerve I. These receptors distinguish odors and produce visceral and emotional responses to the perceived quality of the scent.
The interpretive areas located in the supramarginal and angular gyri provides an integration of the somatic, auditory and visual association areas. It also influences types of cerebration such as detailed memories and memories that require more than one sensory modality. A dominant temporal lobe (usually the left side) generally emerges in the adult where these functions will develop and specialize.
When deficits occur in the dominant temporal lobe as a result of damage to the middle and posterior cerebral arteries or the anterior choroidal artery, severe communication problems result. The person with Wernicke's aphasia exhibits major problems with comprehension and repetition of spoken language.[9,23] Individuals may use jargon or neologisms and maybe unaware that they are speaking nonsense. Reading comprehension may be spared in some individuals.
The occipital lobe is located behind the parieto-occipital sulci and above the cerebellum (Fig 3).[11,23] It is the primary visual receptive and association area of the brain. The primary visual area receives impulses from the retina, transmits them to cranial nerve II and then sends them to the brainstem for further interpretation. It detects spatial organization of vision and is stimulated by sharp borders, colors and contrasts.
The secondary visual area provides complex visual interpretation and perception of form and meaning. This function assists an individual to learn tasks based on visual images and perceptions. The occipital gaze center is also located in this region and predominantly affects eye fixation movements.
Decreased or absent blood supply from the posterior cerebral artery causes deficits in the occipital lobe. This causes visual disturbances end interpretative disorders. Unilateral infarcts cause contralateral visual field abnormalities such as inferior and/or superior quadrantanopia. Contralateral hemianopia results when both regions are involved. Visual field loss may be partial and perception may be altered.
The thalamus, the largest portion of the diencephalon, is located in the ventromedial area of the hemispheres and is connected to the midbrain (Fig 5). It borders and surrounds the third ventricle and is the major integrating center for afferent impulses of the cerebral cortex. All sensory and motor pathways have direct contact with the thalamus except the olfactory pathways.[11,12,14]
[Figure 5 ILLUSTRATION OMITTED]
A thalamic stroke can cause contralateral hemiplegia, contralateral hemisensory deficits and deficits of vertical and lateral gaze. Central post-stroke pain (CPSP) may occur with lesions of the thalamus. Symptoms include diffuse burning, coldness, numbness and tingling, fuzziness, itchiness, aching, throbbing, cramping and tearing sensations.[20,22] Burning is the most common symptom. The pain is usually unilateral and almost always steady in nature.
The hypothalamus is an important area of the brain located anterior and inferior to the thalamus that forms the floor of the third ventricle (Fig 5). It consists of a group of nuclei divided into the anterior and posterior regions. The hypothalamus has many significant functions. The processing of internal stimuli which evokes the autonomic nervous system occurs in the hypothalamus. It functions to maintain blood pressure, heart rate, respiratory rate, body temperature, water metabolism and fluid osmolality, feeding responses, physical expression of emotions, sexual behavior, pleasure-punishment feelings, level of arousal/wakefulness and hormone synthesis.[11,23] In addition, the hypothalamus also regulates salivation, peristalsis, sweating and blood sugar.
Irregularities in hypothalamus function from brain attack include serious clinical manifestations. The individual may experience alterations in temperature regulation, impaired fluid volume status causing diabetes insipidus,[18,24] blood pressure, heart and respiratory rate variations, aversive expressive of emotions and sexual behavior, unusual feeding patterns, impaired blood sugar regulation and impaired gastric motility.[11,14] Because of the vital role the hypothalamus plays in autonomic regulation, its destruction would result in human death.
The pituitary gland lies just below the hypothalamus. It is divided into the anterior and posterior regions, each with specific hormonal control. The anterior pituitary releases prolactin as well as corticotropin, somatotropin, thyrotropic and gonadotropic hormones. Together, with the hypothalamus, the anterior pituitary forms the command center for the endocrine system. The posterior pituitary is primarily responsible for the release of oxytocin and the antidiuretic hormone, vasopressin.
Clinical manifestations of pituitary dysfunction from brain attack include impaired adrenal cortex functioning, alterations in general body growth, disorders of the thyroid, breast development and lactation. Water permeability in the body, vasoconstriction, uterine contraction and the development of primary and secondary sex characteristics are also affected. Of primary importance are the disorders related to vasopressin and thyroid hormones. Vasopressin stimulates the kidney to retain free water by concentrating the urine. If this action is interrupted, diabetes insipidus ensues with uncontrolled free water loss, dehydration and hypernatremia. When thyroid hormones are altered, conditions such as hypothyroidism, hyperthyroidism and the potentially fatal thyroid storm arise. These thyroid disorders influence metabolism, temperature regulation, heart rate, blood pressure, gastric motility and mood.
The basal ganglia are a group of structures made up of brain gray matter called nuclei. These nuclei are located bilaterally in the inferior cerebrum, diencephalon and the midbrain. The main structures of the basal ganglia are the substantia nigra, corpus striatum, caudate nucleus and lentiform nucleus. The main function of the basal ganglia is the production of dopamine and the coordination of muscle movement and posture.
Basal ganglia brain attack may result in disorders related to movement and posture. These include but are not limited to: loss of postural reflexes, tremor, rigidity and involuntary movements such as chorea, athetosis and dystonia. Hemiballismus may also be seen in a patient with basal ganglia infarct.
The midbrain, or mesencephalon, is approximately a one half-inch segment lying between the diencephalon and the pons. It is composed of three layers: the tectum, tegmentum and the cerebral peduncles. The tectum is formed by the superior colliculi which is related to the visual system and the inferior colliculi which are part of the auditory system. The crus cerebri and the tegmentum, also known as the cerebral peduncles, are composed of the corticospinal and corticopontine descending motor tracts. The substantia nigra is located between the tegmentum and peduncles. Its primary function is to synthesize the neurotransmitter dopamine and protect the basal ganglia. Other important structures in the midbrain are the nuclei for cranial nerves III and IV as well as the aqueduct of Sylvius which carries cerebrospinal fluid.[12,23]
Dysfunction in the midbrain may cause several neurological deficits. Motor visual problems may result from alterations in cranial nerves III and IV. Damage to the substantia nigra results in a decreased production of dopamine thus predisposing the individual to Parkinsonism. Auditory and visual reflexes may also be interrupted.[12,23]
The pons is approximately one inch in length and lies below the midbrain and above the medulla (Fig 6). The nuclei of cranial nerves V-VIII are located in this structure and connect the brain to the pons. It's primary function is the transmission of information from the cerebral cortex to the brainstem and between the two cerebellar hemispheres. All of the sensory pathways, reticular formation as well as the corticospinal tract pass through this region. In addition, the pons is an important structure for regulating the respiratory system.[11,12,211]
[Figure 6 and 7 ILLUSTRATION OMITTED]
Clinical manifestations resulting from damage to the pons result in a variety of sensory and motor problems. Alterations in cranial nerves V-VIII may cause the following symptoms: impaired mastication and facial sensations (trigeminal), impaired eye movement (abducens), altered taste, facial expression, eye lid closure and salivation (facial) and problems with equilibrium and hearing (acoustic).[11,15] Deficits in this area also may cause respiratory insufficiency since the rate and character of normal breathing may be affected.
The medulla extends from the spinal cord at the level of the foremen magnum and is located just below the pons and fourth ventricle (Fig 6). The anterior section contains the descending pyramidal tract which contains the lateral and anterior corticospinal tracts. These tracts decussate (except for the anterior tract) in the lower medulla before entering the spinal cord. The lateral portion of the medulla contains the inferior olivary nuclear complex which is important in controlling movement, posture changes and equilibrium. It also contains nuclei for cranial nerves IX-XII. The posterior segment transmits discriminative tactile information, proprioception and vibration sensation to the thalamic nuclei. Also located in this area is the reticular formation. It plays a major role in blood pressure and respiratory regulation as well as the maintenance of arousal and initiation of sleep.
Problems arising in the medulla can be very severe. Damage to this system may result in a persistent vegetative state and contralateral sensory and motor deficits. Other manifestations may include alterations in postural sense, proprioception and vibration in addition to respiratory insufficiency and cardiac/vasomotor dysfunction.[11,23] Dysfunction in the nuclei of cranial nerves IX-XII may also result in problems with swallowing (vague), head and shoulder movement (spinal accessory), tongue movement (hypoglossal), salivation and pharyngeal (glossopharyngeal) function.
The cerebellum is located in the posterior fossa and is separated from the cerebrum by the tentorium cerebelli.[11,12] It is connected to the brainstem by the superior, middle and inferior peduncles. Fissures divide the cerebellum into three lobes: the anterior, posterior and flocculonodular lobes. The anterior lobe receives most of the proprioceptive input, maintains equilibrium, coordinates automatic movements and regulates muscle tone. The posterior lobe coordinates voluntary movements and maintains connections with the cerebral cortex. The flocculonodular lobe integrates with the vestibular system and influences muscle tone, equilibrium and position. The cerebellum is also connected to many afferent and efferent pathways in the brain which provide muscle synergy throughout the body.
Disturbances to the cerebellum result in decrease muscle tone on the ipsilateral side, poor coordination of fine motor movements and problems with gait. Other problems include ataxia, intention tremor, diadochokinesia, dysmetria, hypotonia and asthenia. Another important problem which may occur, especially in a hemorrhagic stroke or other situations leading to increased intracranial pressure, is the downward movement of the cerebellar tonsils through the foremen magnum resulting in a tonsillar herniation and compression of the medulla.
Case Study 1: MCA Brain Attack
JR, a 72-year-old black male, has a history of hypertension and diabetes mellitus. He was found unresponsive at his home by his daughter. Upon admission to the emergency department, he began to awaken but was very confused and agitated. A magnetic resonance imaging (MRI) scan revealed that JR experienced a thrombotic cerebral infarct affecting the frontal and temporal lobes resulting from an occlusion to the middle cerebral artery. Upon a thorough neurologic exam, he was noted to have hemiplegia to the right limbs and expressive aphasia. He also was incontinent of urine. After stabilization, JR was transferred to a step down unit. He continued to be agitated and began to exhibit his nude body to visitors and made several attempts to improperly touch the female nurses. His speech showed some improvement in that he was able to speak slowly but telegraphically. He continued to experience right-sided hemiplegia. About 10 days after his infarct he was transferred to a rehabilitation facility. Over a period of 3 weeks, he regained marginal strength to his right side. His speech improved considerably; however, he still experienced poor judgment, angry outbursts and socially inappropriate behaviors. JR improved enough with regards to his speech and motor function, that he could be considered moderately independent; however, his judgment deficits and social disinhibition (from frontal lobe damage) made him a poor candidate for unsupervised living.
Case Study 2: Brainstem Attack
GP, a 56-year-old white male, has a history of hypertension and obesity. He was admitted to the neurological intensive care unit (NICU) after he experienced a sudden collapse and respiratory arrest at his law office. When emergency personnel arrived at the scene he was unresponsive, with a BP of 86/48 and a rapid thready pulse and absent respirations. He was intubated and ventilated with 100% oxygen. Intravenous (IV) fluids were begun and a dopamine drip was started. He began to arouse; however, was still unable to breathe or move anything except his lips, jaw and eyes. He was transported to the hospital where a MRI of the brain revealed a hemorrhage of the basilar and vertebral arteries affecting the brainstem. His symptoms of respiratory insufficiency, limb paralysis, dysphagia and absent gag reflex were all consistent with the MRI results and the diagnosis of brainstem infarct.
He was intubated and on the ventilator for one week. He remained unable to spontaneously initiate a breath, was paralyzed below the neck and had a diminished gag reflex. Another week passed and his condition remained unchanged.
Since his respiratory status showed no improvement, a tracheostomy was performed and he was extubated, although he still remained on the ventilator. A gastrostomy feeding tube was also inserted because his gag reflex was absent and oral intake was impossible. Attempts at weaning from the ventilator were made, however, they were all unsuccessful. As an alternative to mechanical ventilation, phrenic nerve stimulation was successfully instituted. GP's oxygen saturations were greater than 92% on 35% trach collar oxygen. He was transferred to the step down unit 3 weeks after infarct with a gastrostomy tube, tracheostomy with oxygen and phrenic nerve stimulators. He developed his own methods of communication through lip smacking and eye movements. He fatigued very easily and remained in bed almost exclusively. He experienced episodes of anxiety and depression. Major issues in care centered around his fluctuating respiratory status, immobility, eye care, nutrition and psychosocial concerns. Months after his brain attack, he was transferred to a long-term care facility with no neurological improvements noted since the day of infarct.
Case Study 3: Thalamic Hemorrhage
JS, a 62-year-old retired black male, has a several year history of hypertension and was noncompliant with his antihypertensive medications. On the morning of admission, he awoke feeling drowsy and dull. He also commented to his wife that his left hand felt numb and clumsy. In addition, he had a headache. JS and his wife assumed that he was probably coming down with a flu. After a light breakfast he returned to bed. Sometime later, he began vomiting and complained of an increased headache despite having taken acetaminophen. At this point, his wife brought him to his local doctor for evaluation. Upon examination the doctor found the following symptoms: BP was 172/110, there was a slight weakness in the left arm and leg as well as left downward gaze weakness. An immediate CT scan was performed, identifying a 4 mm thalamic hemorrhage. JS was admitted to the hospital neurological unit for evaluation. His symptoms did not progress. He was discharged to his home two weeks later with no neurological deficits.
Brain attack continues to be a leading cause of illness and disability. Knowledge of anatomy provides the nurse with the ability to understand why brain attack victims exhibit certain deficits. This information is useful for planning individualized nursing care with realistic client goals. In addition, understanding brain anatomy permits the nurse to be an active informed member of the health care discharge planning team. This positively influences client outcomes and assures that individuals achieve their maximum level of functioning.
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RELATED ARTICLE: Earn Two Contact Hours
In this issue, the article Brain Attack: Correlative Anatomy has been approved for continuing education credit. Objectives are listed below. Test questions follow at the end of the article along with further directions.
1. Correlate signs and symptoms with specific vessel involved in brain attack.
2. Understand the function of predominant brain structures.
3. Utilize knowledge of cerebral anatomy to plan nursing care for clients experiencing brain attack.
Questions or comments about this article may be directed to: Linda Testani-Dubour, MSN, RN, CRRN, Shepherd Center, 2020 Peachtree Road NW, Atlanta, Georgia 30309. She is a clinical nurse specialist.
Camille A. Marano Morrison, MSN, RN, is an adjunct faculty member in the department of nursing at York College of Pennsylvania in York, Pennsylvania 17405-7199. Copyright C American Association of Neuroscience Nurses 0047-2603/97/2904/0213$1.25
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|Title Annotation:||includes continuing education post-test|
|Author:||Testani-Dufour, Linda; Morrison, Camille A. Marano|
|Publication:||Journal of Neuroscience Nursing|
|Date:||Aug 1, 1997|
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