 Selective attention to visual or auditory input is common with damage to the temporal lobes (Milner, 1968). Left side lesions result in decreased recall of verbal and visual content, including speech perception. Right side lesions result in decreased recognition of tonal sequences and many musical abilities. Right side lesions can also affect recognition of visual content (e.g. recall of faces). The temporal lobes are involved in the primary organization of sensory input (Read, 1981). Individuals with temporal lobes lesions have difficulty placing words or pictures into categories. Language can be affected by temporal lobe damage. Left temporal lesions disturb recognition of words. Right temporal damage can cause a loss of inhibition of talking. The temporal lobes are highly associated with memory skills. Left temporal lesions result in impaired memory for verbal material. Right side lesions result in recall of non-verbal material, such as music and drawings. Seizures of the temporal lobe can have dramatic effects on an individual's personality. Temporal lobe epilepsy can cause perseverative speech, paranoia and aggressive rages (Blumer and Benson, 1975). Severe damage to the temporal lobes can also alter sexual behavior (e.g. increase in activity) (Blumer and Walker, 1975). Common tests for temporal lobe function are: Rey-Complex Figure (visual memory) and Wechsler Memory Scale - Revised (verbal memory). References: Blumer, D., & Benson, D. Personality changes with frontal and temporal lesions. In D.F. Benson and F. Blumer, eds. Psychiatric Aspects of Neurologic Disease. New York: Grune & Stratton, 1975. Blumer, D., & Walker, E. The neural basis of sexual behavior. In D.F. Benson and F. Blumer, eds. Psychiatric Aspects of Neurologic Disease. New York: Grune & Stratton, 1975. Kolb, B., & Whishaw, I. (1990). Fundamentals of Human Neuropsychology. W.H. Freeman and Co., New York. Milner, B. (1968). Visual recognition and recall after right temporal lobe excision in man. Neuropsychologia, 6:191-209. Milner, B. (1975). Psychological aspects of focal epilepsy and its neurosurgical management. Advances in Neurology, 8:299-321. Read, D. (1981). Solving deductive-reasoning problems after unilateral temporal lobectomy. Brain and Language, 12:116-127. Taylor, L. (1969). Localization of cerebral lesions by psychological testing. Clinical Neurosurgery, 16:269-287. The neurological examination in the setting of trauma is a systematic evaluation of important clinical signs that provide evidence to help determine further management and investigation of the patient's condition. This activity outlines and reviews the basic structure and implementation of a neurological examination in the setting of trauma and describes specific signs that hold clinical significance. Objectives:
The presence of focal neurologic findings or mental status changes is predictive of complications following trauma. A neurologic examination helps to localize and lateralize lesions due to traumatic head or spine injury. Individuals who sustain any type of significant trauma, especially concerning the cranium and spinal structures, should be evaluated to determine the nature and extent of the injury. Neurological findings are most clinically useful in well-oxygenated patients who have normal blood pressure (normotensive), normal blood glucose levels (normoglycemic), and no sedation. This is important as hypoxia (low oxygen in tissues), hypotension (low blood pressure), hypoglycemia (low blood sugar levels), and sedating drugs profoundly alter the signs elicited and severely limit the clinical utility of the exam.[1] In the setting of trauma, a neurologic examination is focused on identifying and assessing the functions of vital portions of the central nervous system. The exam primarily focuses on testing the patient’s mental status, cranial nerves (CN), sensory exam, motor exam, and reflexes. In comatose patients, the exam consists of observing the patient closely and eliciting reflexes to assess the level of cerebral input. For patients with some level of responsiveness, the same basal functions are tested, and additional elements of a standard neurologic exam may be included to further assess findings not obtainable from a comatose patient. The Glasgow Coma Scale (GCS) is a commonly used system for grading the severity of brain injury and serves to supplement the neurologic assessment of patients in the setting of trauma. The GCS, detailed below, is based upon the degree of response in three domains: eye-opening, verbal function, and motor function. The latest terminologies are given in parentheses.[2] Eye Opening (Scored 1-4)
Verbal Function (Scored 1-5)
Motor Function (Scored 1-6)
The combined GCS score ranges from 3 to 15, with a lower score suggesting more severe dysfunction. If an individual component cannot be scored due to some reason (eg. bilateral periorbital ecchymoses or the presence of endotracheal tube), the score should be written as "NT" (Not testable). The GCS assessment can be performed by relatively inexperienced care providers, making it a useful tool in the healthcare setting. Serial or repeat GCS scores should be done to identify changes in neurologic function in the immediate aftermath of a traumatic injury.[3] The GCS Pupils Score (GCS-P) was constructed to include the patient’s responsiveness and pupil reaction, which indicates the brainstem function. For calculating this, the Pupil Reactivity Score (PRS) needs to be calculated initially. If both pupils are reacting to light the PRS is 0, and if both are not reacting to light, the value becomes 2. If one of the pupils is not reacting to light, the PRS becomes 1. The GCS-P is calculated by subtracting the PRS from the GCS total score: GCS-P = GCS - PRS. This score acts as an index of the severity of a patient’s clinical state and prognosis.[4] Mental Status The mental status examination assesses the level of consciousness or alertness, which then permits a more detailed examination of cognitive function. Consciousness is awareness of the internal and external environments. An individual with a normal level of consciousness is “awake” (or can be easily awakened), “alert” (responds appropriately to visual or verbal cues), and “oriented” (knows who and where he or she is and the approximate date and time). Abnormal or depressed consciousness exists on a continuum ranging from mild sleepiness to an unarousable unresponsive state (termed “coma”).[5][6] For patients with significantly depressed consciousness, proper description is crucial, examples are listed below.
Patients who are alert and conscious can then be assessed for cognitive function, which involves complex functions from multiple regions of the brain. Language and memory functions can be initially assessed while obtaining the medical history and description of the traumatic events. Memory function can be tested by the recall of three simple objects (e.g. house, plane, apple) immediately and again 5 minutes later. The cortical function can be assessed by asking patients to subtract 7 serially from 100 (e.g. 100, 93, 86, 79, etc.) or asking patients to spell a simple word both forward and backward (e.g. world). Any overt speech or language disorder should be evident during conversation and initial evaluation. Patients who have suffered significant head trauma may display a peculiar, flat affect, where patients speak in a slow monotone voice without inflection and appear devoid of emotion. Cranial Nerves Twelve total cranial nerves (CN) are routinely tested as part of the neurologic assessment. Examination of the CNs provides crucial information about potential brainstem dysfunction in the setting of acute trauma. The olfactory nerve (CN #1) is not of significant concern in the setting of trauma, and typically it is not tested in this setting. For comatose patients, the optic nerve (CN #2) can be assessed using the “blink-to-threat” test. Simply observe whether the patient blinks in response to a rapid hand movement toward the eyes from different directions. Responsive patients who can easily vocalize their reply may be tested normally for visual acuity using a Snellen eye chart. Additionally, the visual field should be assessed to determine any blind spots or defects. This can be done by asking the patient to fixate on an object straight ahead and to report when a finger can be seen moving in each of the four visual quadrants. It is important to test both eyes separately for visual field defects. Eye vision, position, and movements are key to assessing the function of the CNs. Pupillary responses are one of the most important parts of the neurologic exam in patients with impaired consciousness. The normal pupillary response demonstrates the normal functioning of the optic nerve and the oculomotor nerve (CN #3). First, it is important to note the pupil size and shape at rest. A light should be directed towards each eye twice, first to assess the direct response of the illuminated pupil, and then again to assess the consensual response of the non-illuminated pupil. A normal response to the light stimulus results in constriction (or shrinking) of the pupil. For alert patients, the oculomotor nerve (CN #3), the trochlear nerve (CN #4), and the abducens nerve (CN #6) can be assessed by having the individual close one eye and focus on a finger while it is moved in space. While the patient has his or her eye focused, move the finger in all directions from a central point (horizontally, vertical, and diagonal directions). It is important to closely examine each of the eyes separately and to look for any weak or abnormal movements during this portion of the exam. The same steps can be repeated with both eyes open to assess conjugate gaze functions (when eyes move in the same direction). Any nystagmus (repetitive uncontrolled eye movements), dysconjugate gaze (failure of the eyes to move in the same direction), or fixed deviation of the eyes in a particular direction at rest should be noted. For comatose patients, CN 3, 4, and 6 functions can be assessed, eliciting the normal physiological response called the “oculocephalic reflex.” This is performed by holding the eyes open and rotating the head from side to side or up and down. These maneuvers obviously should not be performed in cases of head or neck injury until appropriate radiological studies have considered possible cervical spinal trauma. The normal oculocephalic reflex is present if the eyes move in the opposite direction of the head movement (e.g., turning the head rightward causes leftward deviation of the eyes to maintain fixation of gaze, sometimes termed “doll’s eyes” movement). In the patient who is comatose, the corneal reflex can be assessed by touching each cornea gently with a cotton wisp that should elicit a bilateral blinking reflex. Facial grimacing should also be noted in response to a painful stimulus, created by rubbing vigorously anterior to the ear or on the supraorbital ridge (bony prominence above each eye). These can be used to assess the function of the trigeminal nerve (CN #5) and facial nerve (CN #7). For patients who are responsive, the trigeminal nerve can be tested by assessing tone in the muscles of mastication and symmetric sensation in all parts of the face. Responsive patients also can demonstrate facial nerve function through symmetric facial expressions like smiling, puffing out their cheeks, clenching their eyes tight, and wrinkling their eyebrows. Any asymmetry should be noted. For the responsive patients, the vestibulocochlear nerve (CN #8) for the auditory function will have partially been assessed through conversation, but direct testing can be done by the rubbing of fingers together right beside the individual’s ear. While performing this action, be sure to ask the patient if the sound is symmetric in both ears. The function of the glossopharyngeal nerve (CN #9) and vagus nerve (CN #10) can be tested in a patient who is comatose or responsive through the gag reflex. The reflex should be symmetric and can be elicited by touching the posterior pharynx or base of the tongue with a cotton swab. The practitioner should have the individual’s mouth open with a light shone on the uvula to visualize its symmetric elevation in response to the tactile stimulus. This can also be elicited by using a suction tube in an endotracheal intubated patient. The accessory nerve (CN #11) can be assessed by asking the patient to shrug their shoulders upwards against the practitioner's resistance, and then asking him or her to rotate the head in both lateral directions against resistance. The hypoglossal nerve (CN #12) is assessed by asking the patient to stick the tongue straight out, to move the tongue side to side, and to push it forcefully against the inside of each cheek. Any weakness or deviation should be noted. Sensory Exam For responsive patients, a sensory exam may be performed. This exam largely relies on the ability of patients to accurately report what they are feeling. This makes interpreting this portion of the exam with certainty a difficult task in some cases. Various types of sensations are brought to the brain via different pathways, and specific patterns of sensory impairment can be a clue to the location or nature of the injury. The skin surface should be systematically tested in all four extremities to determine any pattern of the deficit. A light touch is assessed by applying a very light stimulus, such as a cotton swab, but a light finger touch will often suffice. Pain sensation typically is assessed in two fashions that use a safety pin. The sensation of “sharp pain” can be tested by using the pinprick end, while the sensation of “dull pain” can be tested using the rounded/dull portion. Joint position sense can be tested when the examiner grasps the sides of a distal phalanx (furthest digit segment) of a finger or toe and slightly displaces the joint up or down. The patient, with eyes closed during this part, is asked to report any perceived change in position. Temperature and vibration sensations are not urgently tested in most trauma situations. Motor Exam The motor exam has several steps, including inspection, palpation, and functional testing with tone and strength testing of individual muscle groups. Prior to beginning, observe, inspect, and palpate to detect visible abnormalities. Other findings like muscle twitches, tremors, involuntary movements, or general tenderness should be noted. Before the examination, be sure to assess the patient’s overt injuries and be cautious with the manipulation of any extremities in the context of trauma, to prevent the worsening of any injuries. Before testing strength, some functional tests should be examined. By having the patient hold their arms outstretched with palms upward for several seconds, observe any abnormal inward rotation or downward drift in their hands from their initial position, known as “pronator drift.” Muscle tone is judged by palpation of the muscles of the extremities and by passive movements of the joints by the examiner. Any change in resistance to the movement should be noted. Muscle strength should be assessed in the extremities, neck, and trunk. This is accomplished by providing resistance to the movement of muscle groups in both directions and assessing any indication of diminished strength. The following scale is universally used to describe muscle group strength, rated on a scale of 0/5 to 5/5 as follows:
Reflex Testing The deep tendon reflexes are used to test the functional sensory and motor fibers of a respective spinal level. The stimulus of muscle stretch is created by using a reflex or percussion hammer. A reflex response should be noted immediately following the hammer stimulus. The right and left side response should be compared, with specific attention paid to asymmetries. Reflex responses to stimuli can be described as normal, less reactive (hyporeflexia), or more reactive (hyperreflexia). Deep tendon reflexes often are rated according to the following scale:
Commonly Tested Reflexes Commonly tested reflexes are listed below with the associated spinal level and the method to obtain them. Testing requires a percussion hammer. Biceps reflex (C5/C6) – Hold the patient’s elbow flexed at a right angle with their palm facing upward, and the examiner places a thumb on the biceps tendon (located on the medial side). The examiner then strikes their thumb and looks for a slight flexion at the elbow. Triceps reflex (C7) – With the patient’s elbow supported in the examiner’s hand while letting the forearm hang downward at a right angle, then strike the triceps tendon just above the bony prominence of the elbow. A slight extension of the arm should be noted. Knee reflex (L2/L3/L4) – With the patient sitting on the edge of a table (if possible) and their legs hanging loosely, strike the patellar tendon with the percussion hammer. A slight extension of the knee should be noted. Ankle reflex (S1) – With the patient’s legs hanging loosely, the examiner should grasp the patient’s foot and strike the Achilles tendon. A slight plantarflexion should be noted. Coordination and Gait Coordination and gait usually are tested separately along with individual motor function because cerebellar damage can disrupt gait or coordination while leaving other motor functions relatively intact. First, if the patient is able, assess the patient’s walking motion. Observe the patient’s posture, gait, coordinated automatic movements (swinging arms), and the ability to walk in a straight line. Any abnormal motions or asymmetric movements should be noted. The Romberg test is conducted with the patient standing with heels and toes together with eyes closed. The examiner should stand beside the patient and be prepared to catch them. Patients with certain brain damage may sway or fail to maintain posture with their eyes closed. In the finger-to-nose test, the patient places the tip of a finger on his or her nose and then touches the examiner’s finger, which is placed at arm’s length distance away. This motion should be repeated as rapidly as possible, while the examiner changes the finger location. A lower extremity equivalent of this test is the heel-to-shin test. In this test, the patient places one heel on the opposite knee and then moves the heel up and down along the shin. In both the finger-to-nose and heel-to-shin test, each extremity should be tested separately. General Findings on Exam Fundoscopic examination of each eye is important and should be done to visualize the retinal surface and associated structures. Papilledema (the presence of a swollen or blurred optic disc) should be noted. A subhyaloid hemorrhage (intraocular collection of blood) can occur after direct head trauma and should also be noted. Respiration can be assessed for clues to neurologic function. It is important to note any abnormal or irregular breathing patterns. Head Trauma Findings Below are several findings that may be present in the case of direct head trauma. Bony-Step Off – Palpable discontinuity in the shape of the skull due to displaced fracture. CSF Rhinorrhea – Exudation of cerebrospinal fluid (CSF) (a clear white liquid) from the nose. CSF Otorrhea – Exudation of CSF from the ear. Hemotympanum – Dark blood visible behind the tympanic membrane (eardrum). Battle Sign – Dark bruising visible in the skin overlying the mastoid process (bony prominence just posterior to the ears). Raccoon Eyes – Dark bruising visible in the skin around the eyes.[7] Mental Status A single GCS score is of limited value; it is insufficient to determine the degree of injury after trauma, and it does not have prognostic value.[6] However, serial GCS scores are more valuable clinically when they can be compared over time. An initially low GCS score that stays low or a high GCS that decreases, predicts a worse outcome than a persistently high GCS or a low GCS that progressively increases with time. Additionally, a single high GCS does not eliminate the possibility of serious intracranial injury. Traumatic brain injury (TBI) is a nonspecific term for an injury to the brain due to various injury mechanisms (i.e., blunt, penetrating, or blast injury). TBI can be classified as mild, moderate, or severe; this classification is based on the GCS score. The term “concussion” (interchangeable with mild/minor TBI) is defined as a reversible impairment of neurologic function following head injury. Clinical features of concussion include loss of consciousness during the traumatic injury, “seeing stars” (visual changes), and other symptoms such as a headache, dizziness, nausea, and vomiting.[8] A concussion or mild TBI can result in a transient change in mental status, while a severe TBI can result in extended periods of unconsciousness, and in some cases, can lead to coma or even death. The following is the classification of TBI, based on associated GCS score and mortality rates:
It is important to note that individuals, even with a mild TBI, often can develop Post-Concussive Syndrome (PCS), with headaches, lethargy, mental dullness, and other symptoms that can persist for several months after a TBI.[10] Impaired consciousness can occur in response to damage to the brainstem. Toxic and metabolic factors also are common causes of impaired consciousness because of their effects on these structures and must be explored during early evaluation since trauma can co-occur with intoxication.[5] The presence of flat affect may result from significant head trauma as a result of damage to the frontal lobes, an area of the brain not well-tested by the standard motor and sensory examination.[11] Cranial Nerves Visual field defects can suggest damage to some point along the complex visual pathways. The pupil reactivity, or light reaction, depends on the intact pathway from the retina via the optic nerve (CN #2) to the midbrain then back to the pupillary sphincter muscle via the oculomotor nerve (CN #3). A loss of reaction can be due to injury anywhere along this pathway and can be easily lateralized during an examination. The presence of asymmetrical or abnormally responsive pupils may also be present due to brainstem damage. Normal eye position and movements are dependent on the oculomotor (CN #3), trochlear (CN #4), and abducens (CN #6) nerves. The absence of the oculocephalic reflex (doll’s eye movements) suggests brainstem dysfunction in the comatose patient but can be normal in the awake/conscious patient. Abnormal horizontal eye movements are indicative of damage to the oculomotor nerve (CN #3), abducens nerve (CN #6), or the pons. Abnormal vertical eye movements are indicative of damage to the oculomotor nerve (CN #3), trochlear nerve (CN #4), or the midbrain. Lack of a corneal reflex on either side suggests damage to the trigeminal nerve (CN #5) or Facial nerve (CN #7). Loss of hearing can suggest damage to the vestibulocochlear nerve (CN #8) or crucial middle/inner ear structures. Lack of a gag reflex or an asymmetric response is indicative of damage to either the glossopharyngeal nerve (CN #9) or the vagus nerve (CN #10). Lack of any gag reflex may suggest damage to the afferent portion of the reflex, the glossopharyngeal nerve. An asymmetric elevation of the uvula is more suggestive of damage to one of the two efferent portions of the reflex, the left or right vagus nerve. Significant weakness or asymmetric appearance during testing of the accessory nerve (CN #11) and hypoglossal nerve (CN #12) would suggest damage to these nerves. Sensory, Motor, and Reflexes The sensory exam, motor exam, and reflex testing of the extremities, done in a systematic way, are important to help identify the location and extent of an injury. New onset of sensation loss or sensation changes, muscle weakness, or alterations in reflexes noticed during the post-traumatic neurologic examination can be used in conjunction with knowledge of the key dermatomes and myotomes, to localize impairment to a potential single peripheral nerve, peripheral plexus, or spinal nerve level.[12] In acute traumatic injury to the spinal cord, there is initially a phase called “spinal shock”.[13] This is characterized by flaccid paralysis (decreased muscle tone where the muscles become limp) below the level of spinal cord damage, loss of deep tendon reflexes, decreased sympathetic outflow, and absent sphincter reflexes/tone. The decreased sympathetic outflow leads to relaxation of vascular smooth muscle, dilation of blood vessels, all leading to moderately decreased blood pressure (hypotension).[14] Additionally, decreased sympathetic outflow can potentially lead to a decreased heart rate (bradycardia). Over the course of weeks to months, this initial “spinal shock” phase gradually transitions and ends. After this point, spastic paralysis (increased muscle tone with intermittent involuntary muscle spasms) and hyperreflexia will be present below the level of spinal cord damage. Some sphincter and erectile reflexes may return, often though without voluntary control. General Findings Fundoscopic findings such as papilledema are suggestive of increased intracranial pressure and should be addressed. Subhyaloid hemorrhage is suggestive of a subarachnoid hemorrhage. In the case of direct head trauma, bony-step off will be present in the case of a displaced skull fracture. CSF rhinorrhea often occurs with a base-of-skull fracture involving the ethmoid bone. CSF otorrhea and hemotympanum can occur with a base-of-skull fracture involving the temporal bone. Battle sign and raccoon eyes are also suggestive of base-of-skull fractures.[15] The neurological exam in trauma patients is often done by the trauma team with consultation from the neurologist or neurosurgeon. However, these patients are usually monitored by the neurotrauma nurse with serial GCS. The prognosis of neurotrauma patients depends on the extent of brain injury, the presence of a neurological deficit at admission, comorbidity, age, and the need for immediate surgery. The prognosis is good for patients with a mild head injury, but the recovery can be prolonged. Patients with severe brain injury usually have a guarded prognosis, and many are left with residual neuropsychiatric deficiencies. Evaluation and caring for these patients will have the best results if an interprofessional team of nurses and clinicians provides care. [Level V] |
What should the nurse assess to test the function of the temporal lobe?
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