Neuro - Localization

mizogosa's version from 2017-08-14 20:34


Question Answer
Lethargy/deliriumBicerebral hemispheres
SeizuresCerebral cortex
MemoryThalamus or medial temporal lobes
Hemibody sensory/motorContralateral hemisphere
Visual fieldContralateral, posterior to optic chiasm
LanguageLeft cerebral cortex
NeglectRight cerebral cortex
Spinal cord lesionmyelopathy
Nerve root lesionradiculopathy
Nerve lesionneuropathy
Muscle lesionmyopathy
two functions for the brainstem 1. The first function is that it is a conduit or funnel or tube where axons pass. They are called long tracts. 2. houses cranial nerves that go directly out from it, with one exception: the trochlear nerve
Dominant hemisphereleft
RIGHT CEREBRAL HEMISPHERE lesion1. Left hemiparesis. 2. Left hemisensory loss 3. Left hemineglect or hemiattention 4. Right visual field defect 5. Right gaze deviation/right gaze preference
HEMIPARESIS weakness of the face, arm, and/or leg contralateral to the lesion
HEMISENSORY LOSS sensory loss of the face, arm, and/or leg contralateral to the lesion
HEMINEGLECT OR HEMI-INATTENTION results from injury to the nondominant hemisphere, typically the right parietal lobe. - disorder of sensory perception in which the patient is inattentive to sensory stimuli (e.g., tactile, visual, auditory) presented on the left side of the body although the pathways transmitting sensation may remain intact. In severe cases the patient may deny ownership of the left side of the body, display indifference to or unawareness of a left-sided motor deficit, or neglect the entire left side of his or her environment.
RIGHT VISUAL FIELD DEFICIT A lesion posterior to the optic chiasm in the optic radiations of the temporal and parietal lobes, or in the visual cortex of the occipital lobes, results in a contralateral visual field deficit. The deficit that results is either a homonymous (the same field in each eye) hemianopsia (hemifield visual deficit) or quadrantanopsia (upper or lower quadrant). Patients with visual field defects are often unaware of their deficit and may present with complaints of bumping into things or side-swiping cars on the side of their visual field deficit.
LEFT GAZE DEVIATION/LEFT GAZE PREFERENCEThe frontal eye fields play a role in voluntary saccadic eye movements such as occur when an object darts into one’s peripheral vision. The left eye field in the motor cortex of the left frontal lobe connects to the right horizontal conjugate gaze center in the contralateral brainstem (controls right CN 6 and left CN 3), so they stimulate the eyes to look contralaterally. Therefore, a lesion of the left frontal eye field results in deviation of the eyes to the left. This gaze deviation is specifically called a GAZE PREFERENCE. At rest. the eyes PREFER to deviate to the side of the lesion, but because the cranial nerves themselves are intact, the extraocular movements remain intact. In a patient with depressed consciousness, extraocular movements can be tested by using the Doll’s Eye maneuver (oculocephalic maneuvers) or by cold-caloric testing.
LETHARGY and DELIRIUMresult from BILATERAL BRAIN DYSFUNCTION due to anything that affects both sides of the brain simultaneously – toxic-metabolic abnormalities, cerebral edema, seizures, hydrocephalus, and large strokes or other mass lesions
SEIZURES result from focal or generalized dysfunction of the cerebral CORTEX
MEMORY IMPAIRMENTcaused by either dysfunction of the THALAMUS or of the MEDIAL TEMPORAL LOBES
HEMIBODY SENSORY LOSS and HEMIPARESIS result from contralateral lesions of the parietal and frontal lobes, respectively. The distribution of the deficits assists in localizing the lesion to either the cortex or subcortex. Lesions affecting the lateral surface of the brain result in deficits primarily of the face and arm, while lesions affecting the medial surface result in deficits of the leg. Subcortical lesions often affect face, arm and leg equally since fibers from the medial and lateral cortex come together in the posterior limb of the internal capsule located deep within the cerebral hemisphere.
VISUAL FIELD DEFICIT suggestsa contralateral lesion behind the optic chiasm in the optic radiations (temporal and parietal cortex) or visual cortex (occipital lobe)
APHASIA suggests a left cerebral cortex lesion
HEMINEGLECT suggestsa right cerebral cortex lesion
CROSSED SIGNSipsilateral hemiface and contralateral hemibody deficits are characteristic of a lesion affecting only one side of the brainstem
DECREASED LEVEL OF CONSCIOUSNESSbrainstem dysfunction in the Reticular Activating System which is responsible for wakefulness, makes up much of the core of the brainstem, particularly within the pons and lower midbrain. Interruption of this network of fibers can result in lethargy, stupor or coma.
NAUSEA and VOMITINGbrainstem dysfunction in the medulla oblongata. There are various sources of input to the vomiting center including the Vagus nerve (cranial nerve 10), the Area postrema in the floor of the fourth ventricle, and the vestibular system.
HICCUPS can result from lesions in the medulla, by mechanisms which are unclear.
ABNORMAL RESPIRATIONScenters that control involuntary respiration lie primarily in the pons and medulla. Lesions affecting these areas can result in abnormal respiratory patterns or respiratory arrest.
OROPHARYNGEAL MUSCLE WEAKNESS cranial nerves 9 and 10 innervate the oropharyngeal and laryngeal muscles. Lesions affecting these nerves can result in dysphagia (difficulty swallowing) and dysarthria (difficulty articulating, slurred speech). Dysarthria can actually result from weakness of the lips (labial dysarthria), palate (pharyngeal dysarthria), or tongue (lingual dysarthria).
VERTIGOlesion affecting the vestibular portion of cranial nerve 8
TINNITUS lesion affecting the auditory portion of cranial nerve 8
EYE MOVEMENT ABNORMALITIESbrainstem lesions can affect individual cranial nerves that innervate the extraocular muscles (cranial nerves 3, 4, and 6). The patient complains of DIPLOPIA, and neurologic exam reveals DYSCONJUGATE GAZE. Normally, eye movements are yoked together via brainstem CONJUGATE GAZE CENTERS that make connections with cranial nerves 3, 4 and 6 within the brainstem. The VERTICAL GAZE CENTER is located in the midbrain, while the HORIZONTAL GAZE CENTER lies in the pons. Lesions affecting the conjugate gaze centers on a larger scale result in GAZE DEVIATION due to dysfunction within the gaze center. When gaze deviation is due to cranial nerve dysfunction, it is known as a GAZE PALSY (palsy = weakness).
Cerebellar hemisphere lesions result inIPSILATERAL ataxia.
LIMB ATAXIA lesions in ipsilateral cerebellar hemisphere
TRUNCAL and GAIT ATAXIA lesion in midline cerebellum, or CEREBELLAR VERMIS.
signs of spinal cord dysfunction1) BILATERAL WEAKNESS – paraparesis/paraplegia (both legs) or quadriparesis/quadriplegia (all four extremities) 2) SENSORY LEVEL – sensory loss below a specific level on the trunk occurs with cervical and thoracic cord lesions 3) HYPERREFLEXIA & HYPERTONIA acutely (minutes to days) tone and reflexes may be decreased, but eventually become increased 4) AUTONOMIC DYSFUNCTION: URINARY INCONTINENCE, - CONSTIPATION, - SEXUAL DYSFUNCTION
Cord lesionsintrinsic tend to be painless while extrinsic/compressive tend to be painful and this helps differentiate the possibilities when you are taking a history and examining patients
SYRINGOMYELIA, or SYRINXis a cystic cavitation of the spinal cord. It is most common in the cervical region.
POSTERIOR lumbosacral SPINAL NERVE ROOTS deficitslancinating pain radiating into the legs.
VITAMIN B12 DEFICIENCY myelopathy1. Bilateral lower extremity weakness 2.Vibration and joint position sense loss in both legs 3. from degeneration of both the lateral corticospinal tracts and the posterior columns. 4. aka SUBACUTE COMBINED DEGENERATION of the spinal cord because of the combined degeneration of the lateral and posterior columns.
HIV VACUOLAR MYELOPATHYpresents similarly to vitamin B12 deficiency.
Loss of vibratory sensation and joint position sense in the lower extremitiesSENSORY ATAXIA.
Spinal infarctioneffect anterior columns
HTLV-1 associated myelopathy (tropical spastic paraparesis) 1. chronic progressive demyelinating myelopathy primarily affecting the corticospinal tracts of the thoracic cord. 2. Minor sensory loss may also be present.
Brown sequard syndrome (3)1. Weakness & sensory level to loss of sensitivity to vibration & proprioception ipsilaterally below the lesion 2. Loss of Sensory level to pinprick contralaterally below the lesion 3. Increased deep tendong reflex
PERIPHERAL NEUROPATHYusually more distal than proximal
MONONEUROPATHYoccurs in a single nerve distribution
RADICULOPATHYmyotomal (muscle fibers innervated by a nerve root) pattern of weakness and dermatomal (skin innervated by a nerve root) pattern of sensory symptoms
AXONAL PERIPHERAL NEUROPATHIES patho toxic-metabolic or vascular damage to peripheral nerves that disrupts the transport of nutrients or wastes within the axon.
DEMYELINATING PERIPHERAL NEUROPATHY patho autoimmune conditions → immune-mediated inflammatory damage to the myelin. The most common causes are listed on this slide.
ACQUIRED demyelinating neuropathies1. Guillain-Barré Syndrome/AIDP (acute inflammatory demyelinating polyradiculoneuropathy) 2. CIDP (chronic IDP) 3. Multifocal Motor Neuropathy (MMN) 4. Anti-MAG Syndrome 5. Some toxins
HEREDITARY demyelinating neuropathyCharcot-Marie-Tooth (CMT) Type 1
ACQUIRED axonal neuropathies1. Diabetes mellitus 2. Lyme disease 3. HIV infection 4. Acute intermittent porphyria 5. Lead toxicity 6. Barium salt toxicity 7. Vasculitis (mononeuritis multiplex)
HEREDITARY axonal neuropathiesCharcot-Marie-Tooth (CMT) Type 2