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Brain Injury John M. Lavelle, MS4 OMM Fellow Midwestern University Chicago College of Osteopathic Medicine The Brain Homunculi Sensory Lat Motor Med Med Lat Left Hemisphere Understanding and use of language (listening, reading, speaking and writing) Memory for spoken and written messages Detailed analysis of information Controls the right side of the body Right Hemisphere Judging the position of things in space Knowing body position Understanding and remembering things we do and see Putting bits of information together to make an entire picture Controls the left side of the body Corpus Callosum Functions Connects right and left hemisphere to allow for communication between the hemispheres. Forms roof of the lateral and third ventricles. Dysfunctions Damage to the Corpus Callosum may result in "Split Brain" syndrome. Frontal Lobe PREFRONTAL CORTEX SYSTEM – executive control Dysfunctions Functions attention span perseverance planning judgment impulse control organization self-monitoring and supervision problem solving critical thinking forward thinking learning from experience and mistakes ability to feel and express emotions Loss of spontaneity in interacting with others. Loss of flexibility in thinking. Persistence of a single thought (Perseveration). Inability to focus on task (Attending). Mood changes (Emotionally Labile). Changes in social behavior. Changes in personality. Difficulty with problem solving. Inablility to express language (Broca's Aphasia). Frontal Lobe Functions Motor – responsible for making movements Premotor – selects movements, selection and direction of motor sequences Dysfunctions Loss of simple movement of various body parts (Paralysis). Inability to plan a sequence of complex movements needed to complete multistepped tasks, such as making coffee (Sequencing). Parietal Lobe Functions Processes sensory information Localize touch, pressure, pain, and temperature on the opposite side of the body side Spatial processing Visual guidance of hands, fingers, eyes, and limbs, head Responsive to eye movements Visual motor guidance for reaching and grabbing objects Tactile recognition Information on limb position Localize objects around us Directing movement in space Detecting stimuli in space Distinguishing left from right Parietal Lobe Dominant Parietal Lobe Dysfunctions finger agnosia (can’t tell position of finger with eyes closed) agraphia (trouble writing) R-L confusion acalculia dyslexia errors in grammar apraxia inability to copy movements or make gestures Non-dominant Parietal Lobe Dysfunctions neglect of left side (such as in drawing a clock, left side of drawing a person, left side of words, shaving) unaware anything is wrong or a problem is present constructional apraxia (impaired at combining blocks to build a design or doing puzzles) impaired copying, paper cutting, spatial relations, drawing maps, dressing) Occipital Lobe Functions Vision Dysfunctions Defects in vision (Visual Field Cuts). Difficulty with locating objects in environment. Difficulty with identifying colors (Color Agnosia). Production of hallucinations Visual illusions - inaccurately seeing objects. Word blindness - inability to recognize words. Difficulty in recognizing drawn objects. Inability to recognize the movement of an object (Movement Agnosia). Difficulties with reading and writing. Dominant Temporal Lobe Functions Perception of words Process language related sounds Sequential analysis Increased blood flow during speech perception Process details, individual units Intermediate term memory Long term memory Auditory learning Dysfunctions Decreased verbal memory (words, lists, stories) Difficulty placing words or pictures into discreet categories (Catagorization). Trouble understanding the context of words (Wernicke's Aphasia) Aggression, internally or externally driven Dark or violent thoughts Sensitivity to slights, mild paranoia Word finding problems Auditory processing problems Reading difficulties Emotional instability Non-dominant Temporal Lobe Functions Perception of melodies Pitch/prosody Social cues Reading facial expression Increased blood flow during tonal memory Decoding vocal intonation Rhythm Visual learning Dysfunctions Difficulty recognizing facial expression (Prosopagnosia). Difficulty decoding vocal intonation Social skill struggles Trouble processing music Poor visual imagery Decreased selective attention to visual input Decreased recall of nonverbal items – shapes, faces, tunes Cerebellum Functions Coordination of voluntary movement Balance and equilibrium Some memory for reflex motor acts. Dysfunctions Loss of ability to coordinate fine movements (dysmetria). Loss of ability to walk (ataxia). Inability to reach out and grab objects. Intention Tremor. Dizziness (Vertigo). Slurred Speech (Scanning Speech). Inability to make rapid movements (dysdiadocokinesia). Brainstem Functions Breathing Heart Rate Swallowing Reflexes to seeing and hearing (Startle Response). Controls sweating, blood pressure, digestion, temperature (Autonomic Nervous System). Affects level of alertness. Ability to sleep. Sense of balance (Vestibular Function). Dysfunctions Decreased vital capacity in breathing, important for speech. Swallowing food and water (Dysphagia). Difficulty with organization/perception of the environment. Problems with balance and movement. Dizziness and nausea (Vertigo). Sleeping difficulties (Insomnia, sleep apnea). Limbic System Parts Amygdala: involved in emotion, learning and memory. It is part of a system that processes "reflexive" emotions like fear and anxiety. Cingulate gyrus: processing conscious emotional experience. Fornix: connects the hippocampus to other parts of the limbic system. Hippocampus: plays a significant role in the formation of long-term memories. Functions stores emotional memories modulates motivation controls appetite and sleep cycles promotes bonding directly processes the sense of smell modulates libido Limbic System Dysfunctions moodiness, irritability, clinical depression decreased or increased sexual responsiveness increased negative thinking perceive events in a negative way decreased motivation flood of negative emotions appetite and sleep problems social isolation Basal Ganglia Striatum & Globus Pallidus (caudate and putamen) Functions Initiation and direction of voluntary movement. Postural Balance Emotional motor expression (smiling, frowning, laughing, crying) Dysfunctions Tremor-at-rest Dyskinesia with hypertonia Parkinson’s disease (Loss of dopamine) Dyskinesia with hypotonia Chorea Athetosis Hemiballism (Subthalamic nucleus) Thalamus Thalamus Sensory Function Visual input in the lateral geniculate nucleus (LGN) - lesions result in hemianopia. Auditory input in the medial geniculate nucleus (MGN) - Unilateral lesions have little effect on hearing; auditory information ascends bilaterally. Somatosensory input for position, vibration, pain and temperature in the VPL and VPM nuclei - Lesions cause loss of all sensation on one side of the body. Some patients experience abnormally painful sensations on the anesthetic side - Thalamic Pain syndrome Motor function Interruption of the cerebellar input to VA and VL cause ataxia Interruption of basal ganglia input VA and VL cause akinesia. Cognitive function Arousal: bilateral lesions affecting the intralaminar thalamic nuclei cause unresponsiveness, but the eyes remain open - called coma vigil or akinetic mutism. Memory: Lesions affecting medial thalamic structures cause amnesia. Aphasia, neglect and visuospatial dysfunction Hypothalamus Functions Homeostasis: body temperature, BP, circadian rhythm Endocrine function of pituitary: FSH, LH, ACTH, TSH, Pr, GH, oxytocin, ADH Anterior Hypothalamus: parasympathetic activity Posterior Hypothalamus: sympathetic activity ("Fight" or Flight", stress response. Behavioral patterns: Physical expression of behavior. Feeding center. Pleasure center. Dysfunctions Hormone imbalances Inability to control temperature Uncontrolled BP Diabetes Insipidus (DI) SIADH Emotional abnormalities Decreased libido Excessive thirst Horner’s syndrome Internal Capsule Functions Motor tracts. Dysfunctions Contralateral plegia (Paralysis of the opposite side of the body) Brain Injury Causes Diffuse Axonal Injury (DAI): caused by strong rotational forces of the head, such as with a car accident. The unmoving brain lags behind the movement of the skull, causing brain structures to tear. There is extensive tearing of axons throughout the brain which can disrupt the brains regular communication and chemical processes. Anoxic brain injury: when the brain does not receive any oxygen. Hypoxic brain injury: when the brain receives some, but not enough oxygen. Hematomas: swelling or mass of blood in the brain caused by a break in a blood vessel. i.e: epidural/subdural/subarachnoid or intracerebral hemmorrhage Brain Injury Causes Laceration: or tearing of the brain, usually from a skull fracture or gunshot wound, results in rupture of large blood vessels with bleeding into the brain and subarachnoid space. This can result in hematomas, edema and increased intracranial pressure. Contusion: a visible bruise (bleeding) on the brain. Coup-contrecoup injury: contusions that are both at the site of the impact and on the complete opposite side of the brain. DC-ML System STT System SENSORY ASSOCIATION CORTEX PRIMARY SENSORY CORTEX PRIMARY SENSORY CORTEX VPM VPM SENSORY ASSOCIATION CORTEX WIDESPREAD CORTEX INTRALAMINAR THALAMIC NUCLEI VPL VPL STT SUP. COLL. PAG MES V CHIEF V SpTT SPINAL V RETICULAR FORMATION SRTT TST NC NG NG FAST PAIN & TEMP. ALS 2nd order axons decussate 1-2 spinal segments above their entry level Reflex pathway to ventral horn of cervical spinal cord LEFT NC UE DRGs DORSAL HORN OF SPINAL CORD LE UE DRGs LE SLOW PAIN & TEMP. REFLEX ACTIVITY RIGHT CST System LEFT PMC 6 SMA RIGHT S-I PMA 3,1,2 5,7 M-I 4 Int. Capsule Post. Limb Crus Cerebri Within Basilar Pons CST Pyramid Pyramidal Decussation LCST + ACST awc + - Sensory Information DORSAL HORN OF SPINAL CORD VENTRAL HORN OF SPINAL CORD All muscles, but primarily distal muscles of extremities Primarily axial muscles MOTOR UMNs CORTEX CEREBRAL CORTEX SENSORY CORTEX BASAL GANGLIA contra signs DIENCEPHALON THALAMUS III CEREBELLUM ipsi signs CN LMNs MIDBRAIN IV CST contralateral projection V PONS VI VII ML PPRF hearing, equilibrium VIII IX X XI STT MEDULLA XII DC-ML SPINAL CORD LMNs STT Upper Motor Neurons Paresis (generalized) Increased DTRs Increased muscle tone Spasticity Babinski sign present Clonus may be present Disuse atrophy Guidelines for Medication Usage After TBI Define the problem as objectively and specifically as possible. Use medicines that have some proven efficacy; don’t just use “something” (e.g. Neurontin). Develop clear cut goals and metrics to assist in determining when to stop treatment. Begin low but get to a therapeutic dosing before abandoning usage. Be alert to side effects and undesired effects. Alterations in Cognition and Behavior After TBI Hypoarousal Hypoattention Memory Deficits Depression Delirium Agitation Factors Affecting Cognitive and Behavioral Function After TBI Effects of the TBI Medical Instability Infection Metabolic Disturbances Hormonal/NeuroEndocrine Disturbances Hypoxia Sleep-Wake Disturbances Pain Seizures Factors Affecting Cognitive and Behavioral Function After TBI Medications Cognitive-Impairing Medications Central Acting Antihypertensives (Clonidine) Central Acting Antispasmodics (Tizanidine) GI Agents (H2 Blockers, Reglan) Pain Medications (Narcotics, ? NSAID’s) Sedatives (Benzodiazepines, Sleep Aids) Anticonvulsants (Phenytoin, Carbamazepine, Phenobarbital) Factors Affecting Cognitive and Behavioral Function After TBI Cognitive-Improving Medications Stimulants [Methylphenidate, Dextramphetamine] Amantadine [Symmetrel] Bromocriptine [Parlodel] Selective Serotoninergic Re-Uptake Inhibitors [Prozac, Zoloft, Paxil,Celexa] Combination Antidepressants [Wellbutrin] ? Levodopa-Carbidopa [Sinemet] ? Anti-Alzheimer's Agents [Aricept, Exelon] Coma Intervention Directed Multisensory Stimulation (DMS) demonstrated superior (increased responsiveness, improved RLAS, improved GCS) versus Non-Directed Stimulation (NDS) in RLAS II patients Hall:Brain Injury 1992:6:435-45 Coma Intervention Comatose receiving greater therapy intensity (by 60%) demonstrated a 31% decrease in length of stay. Blackerby:Brain Injury 1989;4:167-73 Cognitive Interventions: Hypoarousal No reliable data to support the efficacy of pharmacologic intervention in the comatose (RLAS I) or vegetative (RLAS II) patient. All you get is a very “alert”-looking comatose or vegetative patient. Small trials do support use of neurostimulants (Amantadine 150 mg bid) in “emerging” patients (RLAS III). Kaelin: Arch Phys Med Rehabil 1996;77:6-9 Cognitive Interventions: Hypoattention Neurostimulants have been demonstrated to improve attention (and +/- function) in responsive patients (RLAS IV-VIII) . Methylphenidate has the most clinically demonstrated efficacy for individuals who have progressed out of coma. Dosing 5-30 mg q 7am and 12 pm. Kaelin: Arch Phys Med Rehabil 1996;77:6-9 Methylphenidate (Ritalin) Modes of Action Release of Dopamine from reserpine sensitive presynaptic pool Braestrup: J Pharm. Pharmacol. 1977, 29: 463 - 470. Inhibition of Dopamine uptake Ferris,Tang: J of Pharmacol. Exp. Ther. 1979, 210: 422 - 428. Inhibition of Monoamine Oxidase Szporny, Gorog: Biochem. Pharmacol. 1961, 8: 263 - 268. Methylphenidate (Ritalin) Pharmacokinetics Peak serum levels are reached within 2 hours (Half life = 24 hrs) Both a wide inter-individual and intra-individual variability in serum concentrations exist MPH levels are not different in responders and nonresponders Gualtieri, CT, et al. J of Amer Acad of Child Psych 1982, 21(1): 19-26. Selective Serotonin Re-Uptake Inhibitors (SSRI’s) Prozac, Zoloft, Paxil, Celexa Inhibit CNS reuptake of Serotonin Activating antidepressants, however somnolence present w/ Paxil at doses >20 mg/day Increase dosage q 4-6 weeks If treating depression, need to commit to 12 month course (or increase recurrence) Bromocriptine (Parlodel) Dopamine receptor agonist Adjunctive treatment for Parkinson’s disease Suggested for low level patients, however limited proven efficacy Dosage: 2.5-15 mg/day in 2 doses Increase dosage weekly High incidence of N/V and Headaches with increasing dosages. Amantadine (Symmetrel) Potentiates Dopamine (mechanism unclear) Adjunctive treatment for Parkinson’s disease (tremor) Dosage: 100-400mg/day in bid dosing (elevated seizure risk above 300 mg/day) Increase dosage weekly Hallucinations dose limiting side effect. Probable efficacy in RLAS III patients. Other Antidepressants [Effexor, Wellbutrin] Effexor and Wellbutrin inhibit Serotonin, NE, and Dopamine reuptake = Activating agents Effexor Dosage: 75-225 mg/day in 2-3 doses (Occasional HTN side effects) Wellbutrin Dosage: 200-450 mg/day in 3 doses (May have worsening effects on agitation) Levodopa-Carbidopa [Sinemet] Increases cerebral dopamine Suggested for low level patients, however limited proven efficacy Side effects can include dyskinesias and cognitive changes Dosage: 400-1600 mg Levodopa/day in 2-3 doses (tablets contain either 100 or 200 mg Levodopa) Anti-Alzheimer's Agents [Aricept, Exelon] Reversible cholinesterase inhibitors = increases cerebral acetylcholine Effective in improving memory in individuals with Alzheimer’s disease Limited research suggests efficacy in TBI patients Extremely expensive, occasional GI side effects Treatment Algorithm: Hypoarousal/Hypoattention Day 1 Define pathology -> CT/MRI, Mechanism of Injury, Secondary BI Assess function: DRS, FIM, RLAS (limited efficacy in RLAS I-III) Assess medical status -> Infections, Oxygenation, Metabolics, Fluid Status, Seizures Remove medications -> H2 blockers, narcotics, central acting anti-HTN/GI, Benzodiazepines, Sleepers Day 1-4 Stabilize/Improve medical status Assess/Improve sleep-wake cycle: Trazadone, Ambien Assess behavior: ABS, Therapy attendance/participation, Attention to Task Treatment Algorithm: Hypoarousal/Hypoattention Day 5-10 Initiate Methylphenidate 5 mg q 7 am and 12 pm, increase 5-10 mg/day to 60 mg maximum Monitor behavior and sleep-wake cycle Day 10-20 If Methylphenidate effective, continue at lowest effective dose for 2-3 weeks, then wean off in 2-4 days If Methylphenidate ineffective by 30 mg/day, then initiate wean and begin new agent. Recommend: SSRI’s may be appropriate if mild but limited response to Ritalin ( if depression is suspected, then Ritalin only effective 4-6 weeks and will need SSRA for 3 months minimum). Cognitive Interventions: Agitation Agitation occurs in >50% of all TBI patients (RLAS IV), however delirium, seizures, pain, hypoxia can also manifest with agitation. True TBI agitation should be treated with environmental and behavioral interventions. Pharmacologic treatment should only be implemented in specific behaviors are identified and goals established. Agitation is defined as an Agitated Behavior Scale score > 21 Cognitive Interventions: Agitation Etiologies Environmental Pain Seizure activity Delirium (meds, hypoxia, metabolic) Inadequate sleep/wake hygiene … or TBI-related confusion Cognitive Interventions: Agitation Treatment Assess for correctable etiology Sleep/Wake Charting Medical Management Behavioral establish desired behavior positive reinforcement shaping structured therapy Agitated Behavior Scale Assess pattern of agitation Documentation Evaluate effectiveness of intervention Physical Restraint Pharmacologic ABS > 28 Agitation: Medications Day 1-3 Use prn for ABS >28 Ativan Risperidone Day 4+ Schedule agents if persistent ABS > 28 Aggression - Beta-Blockers (Propranolol) Restlessness - AED’s (Tegretol, VPA) Emotional lability - TCA’s (Nortriptyline) Wean agent when ABS <21 for 3 days. Cifu: J NeuroRehabil 1995;5:245-254 Post-Traumatic Seizures: Background TBI-related seizures account for 20% of symptomatic epilepsy. Hauser: Epilepsia 1991:32;429-45 PTS accounts for 5% of all cases of epilepsy. Hauser: Epilepsia 1991:32;429-45 Late PTS is present in 4-7% all TBI, nearly 20% rehab TBI, and 35-50% penetrating TBI patients. Yablon: Arch PM&R 1993:74;983-1001 EEG has no predictive value for PTS. Yablon: Arch PM&R 1993:74;983-1001 Prophylaxis for PTS 73% reduction in early PTS and 50% reduction in 1 year PTS in individuals given phenytoin for 1 week post-TBI. No proven benefits to giving prophylaxis >7 days postTBI. Temkin:N Engl J Med 1990:323;497-502 No benefit to use of up to 1 month VPA. Temkin: J NeuroSurg 1999:91;593-600 AANS and AAPM&R recommend 7 days of either PTH or CBZ post-TBI. Prophylaxis for PTS Do not treat seizure in first 24 hours post-TBI longer than initial 7 days, unless status epilepticus. Seizures in the first week should be treated (1 year) unless there is a non-TBI cause evident (infection, hypoxia, metabolic, hydrocephalus). Seizures after 1 week must be treated for at least 1 year. GI Ulcer Prophylaxis Use of H2-Blockers has been demonstrated to decrease ICU-related stress ulceration of the GI tract in specific patient populations (e.g., burns). No specific information in patients with TBI, with or w/o PEG/J tubes. GI Ulcer Prophylaxis Newer H2-Blockers, while expensive, have limited CNS effects. High risk patients (h/o PUD, h/o GERD, comatose, > 65 years old) are appropriate for prophylaxis while in ICU. No clear indication for all TBI patients in ICU. Spasticity Management Treatment should be initiated if the spasticity is limiting function, ROM, or is causing pain. Potential side effects of treatment must be weighed against potential benefits. Spasticity Management: Third Line Systemic medications are effective, but often have systemic side effects: Hepatotoxicity (Baclofen, Dantrium) Generalized weakness (Dantrium) Lethargy (Zanaflex, Baclofen, Valium) Hypotension (Zanaflex) Addiction (Valium) Spasticity Management: Third Line Dantrolene Sodium (Dantrium) Acts peripheral by blocking release of Ca++ from the ttubules of the sarcoplasmic reticulum. Hepatotoxicity is not uncommon. May cause generalized weakness. No central effects. Most often used in Brain Injury and CVA. Start 25 mg qid -> Max 100 mg qid. Spasticity Management: Third Line Tizanidine (Zanaflex) Central acting alpha-blocker. Often causes hypotension. May cause lethargy. very gradual dose increase. Most often used in SCI. Start 1 mg tid -> Max 8 mg tid. Spasticity Management: Fourth Line Phenol (1-10% Aqueous Solution) Direct neurocidal agent, effect lasts for 3-6 months (until nerve regenerates). Works immediately. Eliminates spasticity in specific nerve distribution or muscle. Nerve/muscle motor point (where nerve innervates) must be isolated electrically. Inexpensive. Spasticity Management: Fourth Line Botulinum Toxin (Botox, NeuroTox) Neurotoxin that prevents the release of acetylcholine (Ach) from presynaptic vacuoles at the neuromuscular junction. Produces paralysis of the muscle for 2-4 months. Maximal effects take 2 weeks. Expensive. Spasticity Management: Fourth Line Focal blockade needs to be combined with a structured stretching/bracing program. Focal blockade often reveals underlying connective tissue contractures. If they are “soft”, they can be improved with stretching. If they are hard, surgical intervention is indicated. Guidelines for Medication Usage After TBI Define the problem as objectively and specifically as possible. Use medicines that have some proven efficacy; don’t just use “something” (e.g. Neurontin). Develop clear cut goals and metrics to assist in determining when to stop treatment. Begin low but get to a therapeutic dosing before abandoning usage. Be alert to side effects and undesired effects. Thank You! References Moore, K.L; Agur, A.M. Essential Clinical Anatomy. Lippincott Williams&Wilkins, 2002 Baltimore, MD. Nolte, J; The Human Brain: An Introduction to Its Functional Anatomy, Mosby, 2002 New York, New York. Zasler, ND, Katz, DI, Zafonte, RD; Brain Injury Medicine, Demos Medical Publishing, 2007, New York, New York. www.brainanatomy.net www.neuroskills.com www.uptodate.com