Download CM-Neuro Exam 4 Review Lecture 22-CNS Tumors CNS tumors accounts

CM-Neuro Exam 4 Review
Lecture 22-CNS Tumors
CNS tumors accounts for 2% of all cancers.
 Most common malignant tumor is a GBM (glioblastoma)
 Most common benign tumor is a meningioma
 25% are asymptomatic
 Adults-33% malignant
 Children-65% malignant, leading cause of death, 2nd most common tumor
 Male>female; Caucasian>blacks
Pathogenesis
 Sequential accumulation of genetic aberrations, loss of chromosomes 1p and 19q.
 Defects in PTEN, Rb, p53, and cell-cycle pathways.
 Tumors graded I-IV, higher grade worse the tumor.
 Astrocytomas (which aren’t that bad) can become secondary glioblastomas.
Risk Factors for Developing:
 Exposure to ionizing radiation
 Family history
 Genetic syndromes-neurofibromatosis, tuberous sclerosis, von Hippel-Lindau, etc.
5 yr mortality rates:
 Anaplastic astrocytoma-30%
 GBM-3%
 <14 yrs-62%
 >65 yrs-5%
Diagnosis
 MRI w/gadolinium is the gold standard due to high sensistivity
 CT w/contrast is ok for pt unable to complete MRI.
Clinical Presentation
 Headache-waking from sleep
 Seizures
 Focal neuro deficit
 Confusion
 Memory loss
 Personality changes
 N/V
Herniation Syndromes:
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Uncal herniation (1)-temporal lobe lesion protrudes through tentorial notch
o Structures impinged are PCA, contralateral peduncle and midbrain
o Neuro findings-unilateral dilated pupil from ipsilateral CNIII compression,
oculomotor plasy, homonymous hemianopia (visual loss with respect to
vertical midline), and contralateral hemiparesis
Central herniation (2)-midline tumor compresses basal ganglia, thalamus and
midbrain.
o Neuro findings-small pupils, lethargy, and Cheyne-Stokes respirations
Cingulate herniation (3)-medial frontal lobe tissue is pushed under falx cerebri
anteriorly.
o Critical brian structures not typically involved early on.
o Hernia syndrome is often an asymptomatic precursor to the other
syndromes.
Transcalvarial herniation (4)-also called ‘external herniation.’
o Can be caused by brain edema, pushing outward through fractured skull or
craniotomy.
o May prevent closure from taking place.
Upward herniation (5)-also called upward cerebellar herniation.
o One of the two posterior fossa herniations.
o Cerebellar signs and some midbrain effects.
Tonsillar herniation (6)-posterior fossa tumor compresses downward into foramen
magnum, also called Chiari Malformation.
o Neuro findings-posterior headache, cough, induced syncope, vomiting,
respiratory changes.
o Lhermittes Sign-dyesthesias in the arms and legs with bending neck forward.
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EM management-neuro/neurosurg consult, intubate and hyperventilate, IV
mannitol, dexamethasone, and ICU care.
o Seizures-stabilize the environment, use anticonvulsants, and imaging (MRI
w/gadolinium).
o DVT-duplex US to diagnose in extremities, CT angiography to dx in lung.
Anticoagulation therapy (heparin and lovenox).
Adult Tumors
 Gliomas-loss of heterozygosity for 1p and 19q indicates likelihood of response.
Methylation of MGMT promoter results in better prognosis
o Glioblastomas (60-70%)
 Most common primary brain tumor, medial survival <1 yr.
 Incidence rising in older population
 XRT and temozolamide better than XRT alone.
 Highly vascularized with elevated VEGF expression. Bevacizumab
targets VEGF, and can improve outcomes when combined with chemo.
o Anaplastic astrocytoma (10-15%)
o Anaplastic oligodendroglioma/anaplastic oligoastrocytoma (10%)
o Anaplastic ependymomas/gangliomas-few
 5% of all CNS malignancies
 RT is commonly administered, no standard chemo
 Recurrence has poor outcome
o Grade III and IV
 Meningiomas
o 20-25% of all CNS tumors.
o MRI shows: convexities, parasellar, ‘dural tail’
o Surgery if symptomatic
o Stereotactic radiosurgery for <3 cm
 Germ Cell Tumors
o Germinoma
o Embryonal carcinoma
o Choriocarcinoma
o Teratoma
 CNS lymphoma-rare
o Risk factors include immunosuppression.
o Prognosis better if:
 Age <60
 Good performance status
 Not associated with HIV
 Disease limited to cerebellum
o Treatment Chemo-high dose methotrexate
 Radiation
 Intrathecal chemo
 HIV management w/HAART
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Pituitary adenomas: 10-25% of CNS tumors, either benign, invasive, or carcinoma.
Most are adenomas. Most are asymptomatic.
o Prolactinoma-pituitary tumor that produces prolactin.
 Symptoms: headache, visual field deficits, oligomenorrhea or
amenorrhea, reduced fertility, loss of libido, ED, and galactorrhea.
o Coricotroph-ACTH secreting tumor
 Symptoms: headache, visual field deficits, proximal myopathy,
centripetal fat distribution, neuropsych symptoms, striae (irregular
areas of skin that look like bands), ability to easily bruise/skin
thinning, hirsutism, and osteopenia.
o Somatotroph-Growth hormone secreting tumor
 Symptoms: headache, visual field deficits, growth of hands and feet,
coarsening of facial features, carpal tunnel syndrome, snoring and
obstructive sleep apnea, jaw growth and prognathism, osteoarthritis
and arthralgia, and excessive sweating.
o Thyrotroph-TSH secreting tumor
 Symptoms: palpitations, tremor, weight loss, insomnia,
hyperdefecation, and sweating.
o Non-functioning tumors (endocrine inactive tumor)
 Symptoms: headache, visual field deficits, pituitary insufficiency due
to compression of pituitary stalk or destruction of pituitary tissue by
tumor.
 Rarely ovarian overstimulation, testicular enlargement, or increased
testosterone levels.
 Metastatic
o Complication in 20-40% of CNS tumors
o Multiple mets in 70% of pts.
o Increasing incidence due to MRI imaging and longer survivals improving
chemotherapy.
o Solid tumors:
 Lung-50%
 Breast-15-20%
 Unknown primary-10-15%
 Melanoma-10%
 Colon-5%
Management of CNS Tumors
 Surgery
o Depends on age and performance status
o Proximity to functional areas of the brain
o Feasibility of debulking
o Feasibility of complete resection
o In reoccurrence, time since last resection
 Radiation
o Ionizing radiation damages DNA, apoptosis leads to cell demise, rapidly
growing cells are utilizing nucleotides at a greater rate than dormant.
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o Kid’s brains are very different than adults
o Normal tissue tolerance is looked up in a book, brain doesn’t tolerate well.
o Stereotactic radiosurgery-high dose radiation delivered to small volume
w/in the brain with high precision
o Gamma knife
o Whole brain radiation therapy
Chemotherapy
o Works best when tumor burden is small, fewer cells to kill, more dividing,
and less chance of resistance.
o Combine active drugs making effects additive, decreases chance of resistance
o Traditional agents damage DNA in dividing cells, based on dose
intensity/density.
Immunotherapy
Vaccination therapy
Intrathecal chemotherapy
Lecture 23-Aphasias and Other Cortical Syndromes
Broca’s Aphasia
 Broken Broca’s
 Decreased fluency, good comprehension, poor repetition and naming.
 Inferior frontal lobe (usually left)
 Contralateral weakness can be present
Wernicke’s Aphasia
 Wordy Wernicke’s; word salad
 Good fluency (lots of output, but meaningless), poor comprehension (can’t follow
commands), poor repetition and naming.
 May find homonymous hemianopsia contralateral to lesion
 Posterior superior temporal lobe on dominant side (usually left)
Conduction Aphasia
 Preserved fluency and comprehension, but poor repetition and naming.
 No other neuro findings.
Global Aphasia
 Trouble with all features of language: fluency, comprehension, repetition and
naming.
 Not altered or waxing/waning as would be likely with encephalopathy.
 Unilateral or bilateral weakness can be present.
 Easy to confuse with confusion/encephalopathy
Aphasia Etiology
 Cerebral contusion, subdural or epidural hematoma
 Ischemic or hemorrhagic vascular events
 Ictal or post-ictal deficit with focal seizures
 Mass lesions such as brain tumor, abscess, or toxoplasmosis
 Inflammatory or autoimmune disorders
 Developmental disorders such as language delay or autism
 Degenerative disorders such as Huntington’s, Alzheimer’s, etc.
MCA Syndrome
 Contralateral hemiplegia or hemiparesis (arm>leg)
 Contralateral hemisensory syndrome
 Homonymous heminanopsia
 Contralateral lower facial weakness
 Speech or language abnormality
Alexia-inability to read
 Letter blindness-cannot read letters but can read and comprehend familiar words.
Wrenches’ may have problems with written and spoken language but can read
fluently aloud.
 Parietal-occipital lesions-may not be associated with impaired writing.
o Alexia without agraphia-cannot read but can write on dictation.
o Damage to pathways conveying visual input from both hemispheres to the
angular gyrus.
Gerstman’s Syndrome
 Writing disturbance, finger agnosia, acalculia, r/l disorientation, difficulty spelling
words and understanding spelled words.
 Pure angular gyrus lesion most likely if person doesn’t have a Wrench’s aphasia
 Many patients with alexia with agraphia have a partial or complete gerstman’s
syndrome.
Anton’s Syndrome
 Visual agnosagnosia-pt is blind but denies any difficulty seeing.
 Confabulate about what they see
 Secondary to acute bilateral bi-occipital lesions.
 Agnosognostic component may come from interruption of the thalamic connections
to the right parietal association cortex or right hemispheric dysfunction.
Balint’s Syndrome
 Bilateral parietal-occipital lesions.
 Failure to shift gaze on command, unable to redirect attention voluntarily
 Optic ataxia-failure to reach a target under visual control, appears clumsy.
 Decreased visual attention-affect many peripheral fields resulting in tunnel vision
 Visual simultanagnosia-can’t see whole picture but can name parts.
Internal Carotid Occulsion-Acute
 Contralateral hemiplegia
 Contralateral sensory deficit
 Mutism, aphasia, or dysarthria
 Conjugate eye deviation toward lesion
 Homonymous hemianopsia opposite the lesion
 Horner’s syndrome (ptosis, miosis, and decreased sweating of the face on same
side) ipsilateral to the lesion
 Contralateral lower facial weakness
 Cerebral edema may be life-threatening
Vertebrobasilar artery syndrome
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Locked-in syndrome-lesions in bilateral ventral pons with sparing of the reticular
activating system.
 Characterized by aphonia, quadriplegia, and preserved eye movement.
 Wakefulness maintained
Lacunar Stroke Syndromes
 Pure motor hemiplegia
o Contralateral face and arm > leg weakness
o Mild dysarthria sometimes found
o No vision, language, or sensory change
o Lesion usually in contralateral internal capsule, posterior limb.
 Pure hemi-sensory deficit
o Contralateral face, arm, trunk, and leg numbness, paresthesias and reduction
of pain and temp sensation.
o Lesion usually in contralateral ventral posterior lateral thalamic nucleus.
Posterior Cerebral Artery Syndrome
 Contralateral homonymous hemianopsia
 May have no other symptoms other than visual field cut.
Anterior Cerebral Artery Syndrome
 Contralateral hemiparesis (leg>arm)
 Akinetic mutism-no movement, no speech
 Behavioral or memory disturbance
 Dysarthria or transcortical motor aphasia, similar to Broca’s but repetition is intact.
 Conjugate eye deviation toward lesion.
Lecture 24-Localization in Clinical Neurology
Central Lesions
 Weakness/loss of movement, sensory loss, cranial nerve dysfunction, ataxia,
increased tone/hyperreflexia, language dysfunction, extra movements.
Peripheral Lesions
 Loss of reflexes, atrophy, dermatomal sensory loss, involvement of muscle group
supplied by a particular nerve/nerve root, and weakness/atrophy.
Spinal Cord Innervation Levels
 C7-Middle finger
 T4-nipple line
 T6-bottom of sternum
 T10-level with abdomen
 T12-pubic bone
 S3, S4 and S5-nerves in the genital area.
UMN vs LMN
 UMN
o No wasting
o Increased tone
o Fasciculations absent
o Increased reflexes
o Extensor plantar reflex
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LMN
o Wasting
o Decreased tone
o +/- fasciculations
o absent/decreased reflexes
o flexor plantar reflex
Middle Cerebral Artery
 LOC unusual-usually a sign of impending herniation
 Occlusion at stem-hemiplegia, hemianesthesia, homonymous hemianopia, language
dysfunction.
 Contralateral eye deviation-frontal eye fields, more commonly insula and operculum
 Vertigo-insular involvement
 Visual field disturbance-large infarcts, supplies upper ½ optic radiation
 Neglect-impaired response to contralateral space, usually right lesion
 Apraxia-acquired disorders of execution
Anterior choroidal artery
 Branch of intracranial ICA
 Supplies posterior 2/3 of the posterior limb of internal capsule, retrolenticular
fibers posterior to the IC, posterior optic tract, medial pallidum, tail of caudate,
choroid and thalamus, lateral geniculate body.
 Clinical findings include motor and sensory involvement, mutism, pseudobulbar
state, and other visual deficits.
 1-10% of all infarcts.
Anterior cerebral artery
 Arises as medial branch of birfurcation of the ICA.
 Supplies the whole of the medial surfaces of the frontal and parietal lobes, and
anterior 4/5 of corpus callosum.
 Weakness and sensory loss
o Leg > arm, usually more proximal
o Clumsy or slow movements out of proportion to weakness
o Discriminative senses often affected
o Pain, temp, gross touch less affected.
 Recurrent artery of Heubner
o Supplies head of caudate, anterior inferior part of internal capsule anterior
limb, anterior globus pallidus, uncinate fasciculus, olfactory regions, anterior
putamen and hypothalamus
o Contralateral weakness of face and arm w/o sensory loss, severe
contralateral hemiplegia, cognitive.
Posterior cerebral artery
 Homonymous hemianopia, quadrantanopia (vision loss in one quarter of vision),
palinopsia (images persist after stimulus is gone). Repeated object in the affected
field.
 Visual agnosia-usually alexia w/o agraphia. Difficult naming items presented
visually, able to do when presented tactily or auditory.
 Amnesia-medial temporal lobe, can’t make new memories. May last 6 months.
o Alexia without agraphia-lesion of corpus callosum
o Alexia with agraphia-lesion of angular gyrus
o Language dysfunction
Cerebellar Infarcts
 Superior, anterior inferior, and posterior inferior cerebellar arteries. SCA with PICA
and AICA can also be involved. Brainstem sometimes involved with SCA.
 SCA Syndrome
o Among the most frequent.
o Ipsilateral dysmetria (lack of coordination of movement, overshoot with
hand), ipsilateral Horner’s, contralateral temp and pain loss, contralateral 4th
nerve palsy.
o Unusually choreoathetosis, bilateral hearing loss, and sleep disorders.
o Rostral SCA
 Coma, dysmetria, ipsilateral Horner’s, contralateral pain and temp
loss, and 6th nerve palsy, dysarthria, n/v.
 AICA Syndrome
o Vertigo, n/v, tinnitus, dysarthria
o Ipsilateral facial palsy, hearing and trigeminal sensory loss, contralateral pain
and temp loss.
 PICA Syndrome
o Medulla may be involved, caudal portion of PICA.
 Lateral medullary syndrome-contralateral ataxia, hoarseness,
dysarthria, dysphagia.
 Visual disturbance, ipsilateral facial pain.
 Decreased pain/temperature contralateral
o If medulla isn’t involved then vertigo, ataxia, headache, and horizontal
nystagmus is present.
o May present as labyrinthitis
Lectures 25 & 26-Cortical Syndromes
Dementia-progressive loss of intellectual function with memory loss being the central
primary clinical feature. Abnormalities secondary, with language, spatial processing,
praxis, and executive function.
 Cortical dementia-major symptoms include changes and disturbances in memory,
language, perception and praxis.
o Regions affected include temporal, parietal, and frontal lobes of brain cortex.
o Alzheimer’s disease, diffuse lewy body disease, vascular dementia, and
frtontotemporal dementia are examples.
 Subcortical dementia-behavior changes, emotional problems, slowing of motor
function, disturbance in executive function, and less pronounced memory loss are
key symptoms.
o Thalamus, striatum, midbrain, and striatofrontal projections are affected
regions of the brain.
o Parkinson’s disease, progressive supranuclear palsy, normal pressure
hydrocephalus, Huntigton’s, Creutzfeldt-Jakob and chronic meningitis are
examples.
 Neurodegenerative dementia-involves a primary degenerative disease process with
origin being in the CNS.
o Most common underlying cause of dementia
o Alzheimer’s disease, frontotemporal dementia and diffuse Lewy body disease
are examples of this.
 Other causes of progressive Dementia-origin of degenerative process causing the
dementing illness lies outside CNS or is of non-organic etiology
o Includes structural disease or trauma, vascular disease, etc.
Treatable causes of dementia
 Less than 10% are correctable with treatment.
 Structural processes, infections, metabolic disease, nutritional deficiencies and
psychiatric issues must be considered to rule out reversible or treatable conditions.
 Underlying conditions that can be treated: pseudodementia from depression,
normal-pressure hydrocephalus, thyroid hormone deficiency/excess, thiamine
deficiency, tertiary syphilis, and alcoholism.
Dementia Work-Up
 Electrolytes
 UA
 CBC w/Diff
 Folate and Vit B12
 Liver, Renal and Thyroid fx
 Serologic studies for Syphilis and other studies for chronic infection
 LP
 EEG
 MRI and CT
 Neuropsychological testing
o MMSE (memory and language)
o Clock drawing test (visuospatial)
o ‘Comb your hair’ (praxis)
o Name as many animals as you can in sixty seconds (verbal fluency)
Alzheimer’s Disease
 Complex, progressive disease that destroys cells in the brain. Terminal dementing
illness that results in total care prior to death.
 Most common form of dementia, 5.2 million Americans. Early and late onset
variants.
 6th leading cause of death in US, number of people with this disease is rising.
 Characterized by:
o Gradual memory loss and difficulties in learning.
o Problems with reasoning and judgment
o Loss of language skills and disorientation
o Decline in ability to perform routine tasks
o Changes in personality and behavior
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Costs a lot to care for AD and Dementia pts.
Exact cause unknown, genetic research however, links chromosomes 1, 14 and 21 to
early onset AD, and the ApoE4 gene on chromosome 19 has been linked to late onset
AD.
o Amyloid plaques and neurofibrillary tangles are important components of
interest in this disease process.
o Clumps of beta-amyloid fragments that accumulate between abnormal nerve
cell axons and dendrites forming dense, insoluble structures
o Neurofibrillary tangles are twisted paired strands of hyper-phosphorylated
microtubule associated protein called ‘Tau’ that form inside brain cells
results in inclusion bodies. Correlation between density of tangles and antemortem cognition.
o Both plaques and tangles play a role in blocking neuron communication and
disrupt vital cell processes. Ach is significantly decreased in AD.
o Acetylcholine is an important neurotransmitter in areas of the brain involved
in process of memory formation. Implies that this is related to cognitive
impairment and disordered memory. Current pharmacotherapy targeted at
inhibiting Ach breakdown.
Diagnosing AD
 Clinical diagnosis based on comprehensive history, direct exam of mental/physical
status, lab findings, neuropsych testing and neuroimaging.
 Can be made with 90% accuracy.
 The only way to absolutely confirm is a through post-mortem brain autopsy.
Management of AD
 Nonpharmacological Behavioral Interventions
o Direct behavioral intervention by caregivers
o Safe structured environment
o Activity therapy
o Psychotherapeutic interventions
o Pastoral interventions
 Cognitive Enhancers
o Drugs that work as cholinesterase-inhibitor or glutamate antagonist.
o Tacrine, Donepezil, Rivastigmine, and Galantamine are cholinesterase
inhibitors
o Memantine is glutamate antagonist
o Benefit is modest.
 Medications for Behavioral Symptoms
o Antispychotics
o Antidepressants
o Mood Stabilizers
o Anxiolytics
o Hypnotics
o Pain medications
 Education and support for Caregivers
o Caregiver burden counseling
o Training and teaching for caregivers
o Building family/social support
o Respite services and care assistance
o Legal services
o Medical/ancillary services
o Advocacy groups
 Long Term Care Goals
o Provide AD pt with as much independence and functionality in the least
restrictive setting possible.
o Must be practiced with safety in mind, may have to place pt in a long term
care facility, which requires prep from all involved.
 Modifiable strategies for use in AD
o Mental stimulation
o Physical activity
o Social engagement
o Proper nutrition
o Spiritual growth
Diffuse Lewy Body Disease
 Characteristics
o May overlap with AD and PD.
o Visual hallucinations
o Sensitivity to antipsychotic meds
o More rapid evolution of dementing process.
o Lewy bodies found in brainstem, limbic system and cortex.
Vascular Dementia
 Brain damage secondary to strokes or micro-infarcts.
 Neuroimaging reveals neuronal damage
 Focal neuro deficits are common and there is a supportive clinical time line of
events
 Hx of HTN
 Vascular dementia can overlap with AD causing a mixed dementia
Frontotemporal Dementia
 Pick’s disease is classic form of this type of dementia, which has Pick’s bodies
present.
 Frontal and temporal lobe atrophy.
 May account for up to 5% of dementia.
 Frontal lobe syndrome manifests by inappropriate social behavior.
 Onset is usually earlier than other dementias, occurring during 50s.
 ½ of pts have a family history of similar dementia, being a link between ‘Tau’
protein mutation on chromosome 17.
Parkinson’s Disease
 Dementia occurs in 35-55% of those with PD.
 Impacts executive function much more than language or visuospatial processing.
 Lewy bodies restricted to brainstem.
 Bradyphrenia and bradykinesia are present in PD.
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Depression also common in PD and may worsen cognitive function.
Drugs that treat PD may induce psychosis or delirium, must rule out before
dementia diagnosis.
Normal Pressure Hydrocephalus
 Rare occurrence as cause of dementia, results from obstruction of flow of spinal
fluid.
 Presents with classic triad: dementia, gait disturbance, and urinary incontinence.
 Other features include enlarged ventricles, and elevated ICP.
 Shunt placement is tx, and effective in dementia reversal.
Creutzfeldt-Jakob Disease
 Rare occurrence as cause of dementia with a prion protein being transmissible
agent.
 Presents with dementia, myoclonus, and abnormal EEG.
 Spongiform encephalopathy caused by CJD, rapidly progresses with death in <1 yr.
AIDS
 HIV has direct action on brain.
 Subcortical structures affected more than cortex with bradyphrenia and
bradykinesia.
 No disturbance of language. Forgetfulness, poor concentration and slowed thinking
are common.
 Executive dysfunction and apathy may be more evident as dementia progresses.
Antiviral agents may slow dementia progression.
Head Injury
 Dementing illness that is more retrograde than anterograde. Degree of dementia
correlates with extent of brain damage.
 Usually doesn’t progress unless further trauma occurs. Recovery may take years to
return to baseline.
 Also known as Chronic Traumatic Encephalopathy, Dementia Pugilistica, or Boxer’s
Dementia.
Korsakoff’s Syndrome
 End result of untreated Wernicke’s encephalopathy caused by thiamine deficiency.
 Inability to establish new memory, affected pt’s often confabulate responses.
 Often seen with chronic alcoholism
 Thiamine replacement therapy mandated.
Benign Forgetfulness of Aging
 Aging associated with mild loss of memory, difficulty recalling names and
forgetfulness of dates.
 Poor performance and delay to recall tasks.
 Verbal fluency remains intact, with vocab increasing.
 Dementia is not the normal end-product of aging.
Transient Global Amnesia
 Dramatic memory disturbance that affects pts older than 50 yrs.
 Pt typically has one episode, but more can occur

Characterized by temporal and spatial disorientation with orientation for person
remaining intact.
 Retrograde and anterograde amnesia persist for several hours.
 Pts very anxious/distressed asking same questions over and over.
 Vascular insufficiency to midbrain including hippocampus and midline thalamic
projections may be underlying cause.
Psychogenic Amnesia
 Incosistent loss of resent and remote memory exhibiting an indifference to the
deficit.
 Pt will ask ‘Who am I?’ Disoriented to person.
 Also known as dissociative amnesia.
Pseudodementia
 Dementia syndrome of depression.
 Found in about 5% of pts
 Difficult to distinguish from other causes of dementia, and can coexist with other
dementia.
 Must r/o pseudodementia. Responds to ECT and anitdepressants.
Huntington’s Disease
 Autosomal dominant illness on chromosome 4, CAG repeats.
 Onset 30-50 yrs.
 Causes dementia and chorea within a year of each other.
 Atrophy of cerebral cortex and heads of caudate nuclei.
Subdural Hematoma
 Reversible dementia, most caused by head trauma.
 Sx include headache, confusion, inattention, apathy, memory loss, drowsiness and
coma.
 Lateralizing signs are less common.
Delirium
 Rapid onset, disorganized mental process which causes shit in attention and
awareness.
 Disordered thinking, impaired perceptual discrimination.
 Can be caused by general medical condition, intoxication, withdrawal or other
etiologies.
Lecture 27-Altered State of Consciousness
States of Consciousness
 Alert and awake-normal state of arousal
 Lethargy-fatigued with minimal difficulty maintaining alertness
 Stupor-moderate reduction in alertness, with decreased interest in environment.
Responsive to stimuli
 Obtunded-unresponsivenss with arousal only with painful stimulus. Returns to
unresponsive with removal of stimulus
 Comatose-unresponsive to noxious stimuli.
Consciousness depends on an intact ascending reticular activating system and both
cerebral hemispheres.
Exam of comatose patient
 Verbal responses-oriented, confused, inappropriate, incomprehensible, none at all.
 Eye opening-spontaneous, verbal response, noxious response, none at all.
 Pupillary reactions-present or absent.
o Normal pupils sugges coma not due to structural lesion of CNS
o Unilateral dilation suggests structural injury.
o Bilateral dilated pupils suggests severe brain injury.
o Bilateral midposition pupils unresponsive to light indicates midbrain lesion.
o Pinpoint pupils suggests medication effects, or lesion at pons.
 Corneal response-present or absent
 Spontaneous eye movement-orienting, roving, miscellaneous, none at all.
 Respiratory pattern-regular, periodic, ataxic.
 Motor responses-obeys, localizes, withdrawals, abnormal flexion, abnormal
extension, none
o Purposeful
o Semi-purposeful
o Random, non-purposeful
o Decorticate-legs stiffly extended, arms flexed to chest or neck (toward core)
o Decerebrate-legs and arms stiffly extended (away)
 DTRs-normal, increased, decreased
 Tone-normal, para, flex, ext, flaccid.
GCS
 Eye Opening
o Never-1
o Pain-2
o Verbal-3
o Spontaneous-4
 Verbal Response
o None-1
o Sounds-2
o Inappropriate words-3
o Disoriented-4
o Oriented-5
 Motor Response
o None-1
o Extensor-2
o Flexor posture-3
o Withdrawal-4
o Localization-5
o Obeys-6
Increased ICP detected by deterioration in mental status, pupils, or motor exam
Coma Management:
 Ensure basic metabolic parameters are able to support brain function.
 Check blood gases, H&H, Na, K, Ca, BUN and BGL, and liver enzymes.
Management of increased ICP
 Hyperventilation-lasts 1-2 hrs
 Mannitol-lasts 4-6 hrs
 Mannitol and Lasix are synergistic
 Hyperosmolality with 3% NaCl
DDx of Coma: VITTAMIN D&E
 V-Vascular-infarctions or hemorrhage
 I-Infections
 T-Trauma
 T-Toxic
 A-Anoxic
 M-Metabolic-hypoxia, hypercapnia, acidosis, etc.
 I-Iatrogenic disorders-results from medical procedure/intervention
 N-Neoplasm
 D-Drugs-sedatives, EtOH, tranqs, etc.
 E-Endocrine/Epilepsy/Emotional: hypoglycemia, hyperglycemia, DKA, post-ictal
state, etc.
Coma Copycats
 Locked-in syndrome-pt alert and aware, quadriplegic with lower cranial nerve
plasy.
 Persistent vegetative state-absent cognitive function, but retained vegetative
components. Brainstem preserved.
 Catatonia-mute with marked decrease in motor activity, psych issue.
Prognosis
 No 100% predictability
 Only 15% of trauma comas make satisfactory recovery. Functional recovery
depends on cause of coma.
 Age not predictive of recovery
 Longer the coma lasts, the less likely pt is to regain function.
 Trauma comas do better than nontraumatic
Lecture 28-Progressive Neurodegenerative Disorders
Amyotrophic Lateral Sclerosis (ALS)
 Hallmark is progressive loss of function in both upper and lower motor neurons.
 Median survival is 3-5 yrs, resp failure is COD.
 Males>females
 95% sporadic, 5% familial
 Death of peripheral motor neurons leads to denervation and atrophy of
corresponding muscle fibers; followed by loss of fibers in lateral columns and
replacement by fibrillary gliosis causing gross cord to have an abnormal firmness.
 Clinical Manifestations
o Early-asymmetric distal weakness without sensory abnormalities,
fasciculations, spasticity and wasting.
o Bulbar involvement causes difficulty chewing and swallowing.
o Hyperactive tendon reflexes
o Ocular motility, bladder and bowel sphincters unaffected.
o Later diffuse symmetrical involvement.
 Lab Eval
o CBC and Sed Rate
o CSF exam and culture
o Lyme antibody titer
o Chemistries including glu and calcium
o Thyroid profile
o ANA
o B12, Folate and Vit E levels
o Protein electrophoresis
o Test for heavy metal toxicity
 Imaging
o C-spine Xray to r/o structural problem
o MRI of head and C-spine to r/o other lesions
o Nerve conduction studies will be normal until late stages.
o Electromyography testing will show fibrillations and fasciculations
 World Federation of Neuro Diagnostic Guidelines
o Involvement of bulbar, cervical, thoracic and lumbar areas
o Definite ALS-3/4 areas involved, or SOD1 mutation positive
o Probable ALS-two areas involved
o Possible ALS-Only one site involved and all other causes ruled out.
 Differential:
o Structural lesions in c-spine or foramen magnum
o Infections-lyme disease, tetanus, polio
o Toxicities-lead, aluminum, phenytoin, strychnine
o Paraproteinemias-multiple myeloma
 Treatment
o Supportive care with splints for foot drop and wrist and fingers to assist in
gripping.
o CPAP to assist in ventilation
o Gastrostomy for decreased gag reflex
o Speech synthesizers to help with communication.
 Meds-riluzole shows modest improvement
Multiple sclerosis
 Characterized by inflammation, demyelination and gliosis of the CNS with sparing of
the peripheral nerves. Affects 350,000 in the US. Femals > males. Onset is 20-40yo
 More common in higher latitudes. Migration studies shows increased risk when
people move to high incident areas as children.
 Infection possibly HHV-6, chlamydia, or EBV
 Demyelination with initial sparing of axon results in conduction blocks and slowing
of conduction.
 Clinical Manifestations




o Symptoms often insidious and various depending on location of lesion.
o Complete neuro exam is important, pt may show signs of dysfunction that are
asymptomatic.
o Symptoms can be intermittent and sometimes resolve spontaneously after an
acute flare, making dx difficult to pin down.
o Muscle weakness and clumsiness are common. Spasticity and hyperreflexia
are frequently seen. Exercise induced spasticity of legs may result in gait
disturbances.
o Diploplia due to internuclear ophthalmoplegia from CN VI palsy.
o Optic neuritis seen in 30% of MS pts, and presents with decreased central
field of vision. Usually monocular, may have peri-orbital pain prior to vision
loss. Fundoscopic exam may see optic disc swelling.
o Sensory sx: pain, paresthesias, hyperesthesia.
o Bladder dysfunction-frequency, urgency or incontinence.
o Constipation
o Sexual dysfunction
o Cognitive dysfunction-impaired memory, attention and difficulty switching
tasks.
o Depression-may be reactive or endogenous
o Fatigue-90% of pts, may be related to sleep disturbances, increased effort
with ADLs or depression.
Course of Disease
o Relapsing/remitting MS-85%
 Discreet attacks
o Secondary progressive MS
 Starts as relapsing/remitting MS then increasing deterioration and
less attacks
o Primary progressive MS-15%
 No attacks, gradually worse and worse
o Progressive/relapsing MS
 Progressive with rare attacks
Diagnostic Tests
o MRI of brain and thoracic spine
o CSF analysis shows elevated protein and WBCs
Diagnosis Criteria
o Documentation of 2 or more episodes of symptoms and 2 or more sigs that
show pathology in non-contiguous white matter tracts of CNS
o Symptoms must last >24 hrs and episodes separated by 1 month
o Abnormal MRI, EP and CSF findings support diagnosis
Treatment
o Acute episodes require IV coritcosteroids for 3-5 days, then oral taper for 2
weeks. Plasmapheresis if not responsive to steroids.
o Disease modifying drugs can be helpful to prevent exacerbations
 Interferon-immunosuppressive
 Glatiramer Acetate-induces suppressor T-Cells
 Natalizumab-mab prevents lymphocyte adhesion
o Symptomatic therapy
 Ataxia/tremor-clonazepam
 Spasticity-diazepam, dantroline, cyclobenzaprine
 Pain-gabapentin, amitriptyline
 Bladder dysfunction-oxybutynin and hyoscyamine
 Prognosis
o Difficult to estimate. Better prognosis if <2 episodes in 5 yrs.
o 80% require assistance with ambulation and ADLs after 25 yrs
o Mortality is related to complication of infection in a debilitated pt.
Guillain-Barre Syndrome
 Clinical Manifestations
o Rapidly progressive ascending areflexive motor paralysis. Sensory deficits
are mild.
o Evolves over a few days and peaks 2-3 weeks.
o Fever is rare, muscle pain in neck, back and shoulders.
o 30% require ventilator support
o Autonomic involvement is common.
o 70% of cases occur 1-3 weeks after an infection or immunization:
 campylobacter jejuni
 Mycoplasma pneumoniae
 CMV
 EBV
 Influenza vaccines-swine flu 1976
 Etiology
o Surface glycoproteins of infectious agents cross-react with gangliosides on
the myelin sheath.
o Activated B-cells produce antibodies that cause demyelination and
conduction block in nerve.
o Complement is deposited on outer surface of myelin sheath and leads to
degradation.
 Evaluation
o Elevated CSF protein, w/o elevated WBCs
o EMG shows axonal-reduced amplitude of action potentials, conduction
slowing due to demyelination.
 Diagnostic Criteria
o Required:
 Progressive weakness of 2 or more limbs
 Areflexia
 Disease course less than 4 weeks
 Exclusion of other causes
o Supportive
 Symmetric weakness
 Mild sensory involvement
 Absence of fever
 Typical CSF
 EMG evidence of demyelination
 Treatment
o Initiate IV immunoglobulin G or plasmapheresis ASAP for 5 days.
o Supportive care includes ventilator support, heart arrhythmias, BP, nutrition,
frequent turning, DVT prophylaxis
 Prognosis
o 85% have full recovery in several months to a year
o 5-10% can have relapse
o <5% mortality, death usually related to pulmonary complications and
infection.
Myasthenia Gravis
 NM disorder causing weakness in skeletal muscle. Autoimmune attack on NM
junction causes a decrease in Ach receptors.
 Pathophysiology
o Reduction and flattending of AChR sites at the postsynaptic membrane,
prevents propagation of AP.
 Clinical features
o Females (20-30yrs)>males (50-60yrs)
o Characteristic patter on muscle weakness and fatigability.
o Weakness of CN muscles early in disease, worse after repetitive use and
better after rest.
o Weakness of eyelids and extraocular muscles causes ptsosis and diplopia
o Weakness with prolonged chewing
o Weakness in tongue and palate causing nasal/mushy speech.
o Dysphagia can cause aspiration
o If intercostal or diaphragm are affected then pt is in trouble
 Diagnosis/Eval
o Neuro exam shows weakness with repetitive tasks
o Normal DTR’s
o Normal sensation
o Normal CT or MRI of brain
o Antibodies to AChR and MuSK
o Repetitive nerve stimulation will show decreased potentials and the fatigue
of muscle fibers.
o Anticholinesterase testing-edrophonium (muscle weakness improves) and
neostigmine
 Treatment
o Anticholinesterase medications
o Thymectomy
o Immunosupressive therapy
o Plasmapheresis
o IV Immunoglobulin

o Avoid these durgs: aminoglycosides, quinolones, macrolides,
nondepolarizing muscle relaxants, beta-blockers, botox, quinine, magnesium,
and penicillamine
Prognosis
o Most pts live full productive lives.
o Active phase-peak symptoms with fluctuations for 2-3 yrs
o Stable phase-may worsen with infection or med changes.
o May have a remission phase, with or without meds.
Lecture 30-New Onset Seizures in Peds
Status Epilepticus-continuous seizure activity without regaining consciousness lasting >30
minutes (historical); >5 minutes (real life).
 Convulsive SE
 Nonconvulsive SE
 Refractory SE-failed to respond to therapy and lasts >60 minutes
 Febrile SE-seizure lasting >30 minutes plus occurs between 6-60 months old, temp
>38 degrees C, no CNS or metabolic cause, absence of prior non-febrile seizures.
Etiology of Seizure
 GRAND MALS
 G-Glucose
 R-Rising BP
 A-Alcohol/anatomic
 N-Neoplasm/neuro infection
 D-Drugs
 M-Metabolic
 A-Arterial Disease
 L-Electrolytes
 S-Subdural/SAH
Partial Seizures-focal seizure only involves part of the brain.
 Simple Partial-only seizure in which level of consciousness is not altered or lost.
o Seizures caused by abnormal activation of a limited number of neurons, signs
and symptoms that allow localization of epileptic focus.
o Short 10-20 sec
o Child is conscious and able to verbalize
o Aware and able to remember seizure
o Treat with anti-epileptics, resolves in adolescence.
 Complex Partial
o Frequently starts with aura followed by an alteration in consciousness, then
stereotypic behavior or vocalizations.
o Automatisms can continue in postictal phase.
o Child not always aware of seizure, and won’t remember episode.
o Treat with AEDs.
 Partial w/ Secondary Generalization
o Partial seizure generalizes secondarily if epileptic activity propagates to
entire brain.
Generalized Seizures-involves whole brain, caused by global activation of neurons and
always impairs consciousness. Motor changes and EEG abnormalities observed bilaterally
in a synchronous, symmetric pattern.
 Absence
o Formerly referred to as petit mal seizures.
o Characterized by frequent, abrupt loss of consciousness accompanied by
eyelid flickering that ends abruptly with resumption of activity.
o Never have an aura or postictal period.
o Can be induced by hyperventilation or photic stimulation
o Typical vs. atypical types.
 Typical: abrupt onset, eye flickering, short duration, idiopathic
generalized epilepsy. 3 cycles of 3 Hz per second.
 Atypical: gradual onset, other prominent symptoms including aura
and automation, long duration (several minutes), and focal pathology
or symptomatic epilepsy.
 Myoclonic
o Brief contractions (non-rhythmic) of a muscle, muscle group, or several
muscle groups.
o Action, noise, startle, photic stimulation, or percussion can sometimes
provoke the seizure.
 Clonic
o Jerking (rhythmic), that is asymmetric and irregular.
o Occur more frequently in neonates, infants or young children.
 Tonic
o Sustained muscle contraction without clonic phase.
o Occur at any age and are associated with diffuse cerebral damage, often seen
in kids with Lennox-Gastaut syndrome.
 Tonic-Clonic-grand mal seizure
o Characterized by three successive phases:
o Tonic phase-lasts 10-30 seconds, contractures.
o Clonic phase-lasts 30-60 seconds, rhythmic jerking.
o Postictal phase-lasts 2-30 minutes, state of confusion and fatigue.
 Atonic
o Characterized by loss of muscle tone, ‘drop attacks.’
o May involve only the tone of head and neck. These kids wear helmets.
Pediatric Seizure Syndromes
 Benign Rolandic Seizures (Benign epilepsy of childhood)
o Onset age 5-10 yrs.
o Infrequent self-limited seizures involving a facial or arm motor seizure;
throat tingling is characteristic.
o Child is conscious but cannot speak.
o Occur at night while child is asleep
o Can be associated with migraines.
o Dominant trait, look for family history
o Often left untreated.
o Spontaneous remission by adolescence is typical.
o BECTS-Benign childhood epilepsy with centrotemporal spikes
 Juvenile myoclonic epilepsy (Janz Syndrome)
o Onset is 12-16 yrs.
o Myoclonic jerks upon awakening that diminish through day.
o Most children develop tonic-clonic seizures.
o Linked to defects on chromosome 6P (AD)
o Treatment with valproic acid
o Excellent prognosis but lifelong treatment is required.
 Temporal Lobe epilepsy (TLE)
o Onset in late childhood and adolescence
o Typical seizure is partial complex seizure with secondary generalization
o MRI may show low grade tumor, cortical malformation or mesial temporal
sclerosis
o Treatment with AEDs and sometimes surgery
 Acquired Epileptic Aphasia (Landau-Kleffner Syndrome)
o Onset at 3-6yrs
o Characterized by abrupt loss of previously acquired language in children.
o Cortical auditory deficit.
o Some pts develop generalized seizure.
o Etiology is unknown.
o Treatment with AEDs, steroids, and surgery.
 Lennox-Gastaut Syndrome (LGS)
o Onset at 3-10 yrs
o Mix of seizures including myotonic, tonic-clonic, atonic, absence and partical.
o Treat with valproic acid, and other AEDs
o Prognosis is poor, most children have Mental Retardation and behavioral
problems.
 Infantile Spasms (West Syndrome)
o Onset in infants, from 4-6 months.
o Sudden flexion or extension of neck, back and extremities.
o Occur in clusters lasting 10-30 sec
o Occur when infant is waking up or going to sleep.
o Loss of developmental milestones after onset of seizures.
o Seizure type may change with age.
o Associated with tuberous sclerosis
o First line of treatment is with ACTH.
o Prognosis based on amount of developmental delay.
Diagnostics
 First Tier
o Seizure semiology (H&P)
o Interictal EEG
o Video-EEG
o MRI
 Second Tier
o Invasive EEG (subdural electrodes)-electrical map
o Single Photon Emission CT (SPECT)-blood flow map
o Magnetoenceophalography (MEG)-functional map
o PET-metabolic map
Treatment
 Antiepileptic drugs (AEDS)
 Steroids: ACTH (West syndrome) and prednisone (Landau-Kleffner syndrome)
 IVIG
 Ketogenic Diet
o Initial period of fasting, followed by a diet with 3:1 or 4:1, fat:nonfat ratio
o Mechanism unknown
o Ketosis elvates levels of beta-hydroxybutyrate and acetoacetate. Higher
levels=better seizure control.
o Continued for 2 yrs in children who have good sz control.
o Responders can dramatically decrease or discontinue anticonvulsants.
o Contraindicated with carnitine deficiency.
o Metabolic work-up may be needed before starting diet.
o May not be tolerated due to lack of palatability
o Valproic acid can’t be used with diet.
o Atkins and low-glycemic index diets are easier to start
 Epilepsy Surgery
o Vagal nerve stimulator
 Used for intractable epilepsies and for seizures of diffuse or multifocal
anatomic origin that cannot be resected.
 Electrical signals applied to left vagus nerve.
 Side effects: cough/voice change
o Focal resection
 Resect epileptogenic zone
o Hemispherectomy
 Used for diffuse hemispheric lesions
o Multiple subpial transection
 Connections of epileptic focus are partially cut without resection.
o Corpus callostomy
 Used for drop attacks
 Counseling
o Education about disease
o Not required to report epileptic pt to DMV
o Seizure-free period of 6 months is required before driving is allowed.
o Swimming in rivers, lakes or sea and underwater diving are prohibited, pools
are okay
o Pt with epilepsy should remain under constant supervision when swimming
Lecture 31-Seizure and Epilepsy in Adults
Mechanisms of Seizure
 Excitation-too much, neurotransmitter glutamate and aspartate.
o Ionic-inward Na and Ca currents.
 Inhibition-too little
o Neurotransmitter-GABA
o Ionic-inward Cl and outward K currents
Absence vs. Complex Partial Seizures
 Absence:
o Symptoms of generalized epilepsy.
o Last only seconds, can occur 100 times or more per day
o Start and end abruptly, no postictal confusion
o Produce little or no abnormal motor activity
o Misdiagnosed as daydreaming or inattention
o EEG shows 3 Hz spike and wave bilaterally
 Complex Partial Seizures
o Symptoms of focal epilepsy
o Lasts more than a minute
o Cause alterations in consciousness
o Followed by postictal confusion
o Most frequently originate in temporal lobe and involve limbic structures
o EEG shows focal spikes and sharp waves unilaterally
Jacksonian March
 Simple partial seizures, motor signs begin with clonic or tonic movements of a
discrete body part.
 Muscles of face and hands often involved
 Seizure begins in primary motor cortex and spreads to involve rest of precentral
gyrus, clonic movements progress in orderly sequence (Jacksonian march) that
reflects the motor cortex homunculus representation:
o Thumb to fingers to face to leg.
Tonic Clonic Seizure
 Tonic phase-occurs abruptly, inclues limb extension bilaterally. Air is ejected
forcefully against tightend vocal cords, responsible for ‘epileptic cry’
 Clonic phase-synchronous muscle contraction
Seizure is a symptom and epilepsy is a syndrome, disease or disorder.
Classification of Epilepsy
 Localization-related (focal, local and partial) epileptic syndrome
o Idiopathic-age-related onset
 Benign childhood epilepsy with centrotemporal spikes (rolandic
epilepsy)
 Childhood epilepsy with occipital paroxysms
o Symptomatic
 Chronic progressive epilepsia partialis continua of childhood.
 Frontal lobe epilepsies
 Occipital lobe epilepsies
 Parietal lobe epilepsies
 Syndromes characterized by specific modes of precipitation
 Temporal lobe epilepsies
o Cryptogenic-symptomatic with unknown etiology
 Generalized epileptic syndrome
o Benign familial neonatal convulsions
o Benign myoclonic epilepsy of infancy
o Juvenile myoclonic epilepsy
o Epilepsy with generalized tonic-clonic seizures on awakening
o Epilepsy with generalized tonic-clonic seizures only
o Absence syndromes
o Lennox-Gastaut syndrome
o Progressive myoclonic epilepsies
o West Syndrome
 Undetermined as to whether focal or generalized
 Special syndromes
Antiepileptic drugs
 Mechanism
o Na inactivation-phenytoin, carbamazepine, lamotrigine, topiramate, valproic
acid
o GABA activation-gabapentin, topiramate, phenobarbital, valproic acid,
benzos
o Ca inactivation-ethosuximide
 Many AEDs involved in P450 system and cause significant drug interaction.
o P450 inducers: barbiturates, phenytoin, carbamazepine
o P450 inhibitors: Depakote is a weak inhibitor
Eval of First Seizure
 H&P
 Blood tests: CBC, electrolytes, glucose, calcium, magnesium, phosphate, hepatic and
renal function (LFTs, BUN, Creatinine)
 LP if meningitis or encephalitis suspected
 Blood or urine screen for drugs
 EEG
 CT or MRI of brain
Seizure Precipitants
 Metabolic and electrolyte imbalance
 Stimulant/other proconvulsant intoxication
 Sedative or EtOH withdrawal
 Sleep deprivation
 Antiepileptic medication reduction or inadequate AED treatment
 Hormonal variations
 Stress
 Fever or systemic infection
 Concussion and/or closed head injury.
Seizure Risk Factors
 Family history
 Hx of febrile seizures
 Hx of head trauma
 Hx of meningitis
 Hx of stroke
Causes of Breakthrough Seizures (while on AEDs)
 Metabolic and electrolyte imbalance
 Stimulant/other proconvulsant intox
 Sedative or ethanol withdrawal
 Sleep deprivation
 AED reduction or inadequate tx
 Hormonal vairiations
 Stress
 Fever or systemic infection
 Concussion and/or closed head injury
Status Epilepticus-seizures that last for 5-20 minutes
 Mortality is 3-20%
 Treatment plan:
o Lorazepam first 1-2 min
o Immediately followed by phenytoin or fosphenytoin
o After 20 min seizure continues, add additional phenytoin or fosphenytoin
o After 30 min…add phenobarbital
o After 50 min…increase phenobarbital
o After 60 min…anesthesia with midazolam or propofol
 Neuro emergency, pt’s who have first episode of status epilepticus are at risk for
future episodes.
 Outcome is usually worse the longer the episode lasts.
 12-30% of pts with a new diagnosis of epilepsy first present in status epilepticus
Pseudoseizures
 Represents 15-30% of seizures diagnosed. Common symptom of conversion or
somatization disorder.
 May occur in individual who has epileptic seizures.
 Occurs without accompanying changes in EEG. Diagnosis made by recording typical
events with video EEG.
 Post-ictal confusion may be absent.
 Evidence of loss of motor control during seizure.
 Maintain high degree of suspicion when seizures are refractory to therapy, or when
atypical features are present.
Lecture 32-Ethical Decisions in Neuro
Palliative vs. Hospice Care
 Palliative:
o Addresses goals of care and focuses on quality of life, family support and
symptoms management
o Can begin with onset of symptoms from a serious, life-limiting disease
 Hospice
o Specific type of palliative care provided when pt is terminally ill.
o Provide team based support services to pt, family and caregivers in home or
an institution.
Principles of Palliative Care
 Respect goals, likes and choices of the dying
 Looks after the medical, emotional, social and spiritual needs of the dying
 Supports the needs of family members
 Helps gain access to needed health care providers and appropriate care settings
 Builds way to provide excellent care at the end of life.
Palliative care pts live longer, because they are getting the care they need!
Hospice team:
 Family member is primary caregiver
 Interdisciplinary team:
o Patient’s personal physician
o Hospice physician/medical director
o Nurses
o Home health aides
o Social workers
o Clergy and bereavement counselors
o Volunteers
Levels of Care
 Routine home care-most common type of hospice service, may be in private home,
assisted living facility or long-term care facility
 General inpatient hospital care-uncontrolled distressing physical symptoms,
psychosocial problems, provided in a variety of settings.
 Continuous home care-pt’s qualify for inpatient care but desire to remain in home.
Care provided 8-24 hrs per day by LPN or RN.
Dementia
 Affects 10% of population by age 65
 Affects 50% of population by age 85
 Hospitalized pts with dementia have a 6x higher mortality rate than those w/o
dementia.
o Contributing factors: immobility, loss of ability for self care, anhedoniapleasure from activities or hobbies is loss, decline in coordinated tasks (gait,
continence and swallowing).
 PEG tubes are not supported in response to dysphagia and aspiration risk. Some
studies indicate higher aspiration risks and higher mortality rates in pts with
feeding tubes, compared to those without.
 Other studies suggest that enteral feeding does little to improve nutritional status or
pressure ulcer rates.
 Benefits of not placing PEG tube: focus on other needs of pt (frequent oral care,
intimacy of hand feeding for family, pleasure foods-ice cream).
o Less choking on oral secretions
o Fewer diaper changes
o Less skin breakdown
Making Medical Decisions:
 Capacity determined by primary physician. Doesn’t require legal or psychiatric
expertise.
 Competence is a judicial determinance. Required when assessing a pt’s global
decision making capacity for non-medical issues.
 Pts have the right to refuse life-sustaining medical treatments. Based on
philosophical concept of respect for pt autonomy.
 Pts without decisional capacity have same rights as mentally competent pts.
Treatment should conform to what pt would want on basis of written or oral
advanced care planning. If pt’s beliefs are unknown should be based on known
values, and previous choices.
 If all else fails make a decision in best interest of pt.
 Advanced care planning: pt develop and indicate preferences for care and choose a
surrogate to act on their behalf.
o Should be discussed regularly before acute event occurs.
 If you don’t agree offer empathy, and thoughtful exploration of all possibilities.
o If it violates your professional integrity, refer to another physician but don’t
abandon pt. Ethics consultation may be an option.
Physician Assisted Suicide
 Oregon is only state legal, provide pt with a prescription of a drug that a known
overdose will occur if taken too much of.
o Must be an adult and legal resident of Oregon
o Diagnosed with terminal illness, life expectancy less than six months
o Make two oral requests to PCP separated by 15 days
o Provide written request to physician, signed in presence of two witnesses.
o Prescribing physician and consulting physician must confirm diagnosis and
prognosis and determine whether pt is capable of making decision.
o Prescribing physician must inform pt of alternatives
o Prescribing physician must request pt to inform next of kin.
 Highly controversial, under this law not considered suicide. Prohibits euthanasia.
Telling the Pt the Truth
 Code of ethics requires honesty to pt, regardless of family request.
 Must respect pt, their autonomy!