Neuro Diseases / Disorders Flashcards
1
Q
epilepsy
A
disorder with intermittent, unpredictable, repeated, unprovoked seizures
2
Q
seizure
A
physical manifestation of abnormal electrical activity in the brain - uncontrolled coordinated firing of neurons in certain area of brain with or without change in level of consciousness
3
Q
convulsion
A
type of seizure with activity in area of brain that controls movement, includes involuntary muscle movement
4
Q
epilepsy facts
A
1% of US pop, 2/3 starting in childhood especially during first year of life, increases again after 60, most common pediatric neurological disorder
5
Q
EEG
A
electroencephalogram, ambulatory EEG - cap with electrodes that records activity over time and shows activity disturbances even if a seizure does not take place, Tx based on type of seizure
6
Q
normal EEG
A
coordinated peaks and valleys
7
Q
generalized epilepsy EEG
A
constant peaks and valleys
8
Q
generalized seizures
A
generalized bilateral, symmetrical, no local onset, includes grand mal and petit mal
9
Q
gran mal seizure
A
type of generalized seizure, bilateraly, symmetrical, no focal onset, tonic, clonic, tonic-clonic
10
Q
petit mal
A
type of generalized seizure, loss of consciousness only
11
Q
complex petit mal
A
type of generalized seizure, mostly loss of consciousness with brief tonic / clonic / automatic movements
12
Q
tonic
A
tensing of muscles
13
Q
clonic
A
as in clonus, contracting and relaxing muscles
14
Q
partial / focal seizure
A
local onset, includes simple or complex focal seizures
15
Q
simple focal seizure
A
no loss of consciousness / altered psychic function, includes motor, autonomic, pure psychic (bizarre behavior)
16
Q
motor simple focal seizure
A
focal onset, no loss of consciousness / altered psychic function, frontal lobe origin, tonic, clonic, tonic-clonic, benign childhood epilepsy
17
Q
complex focal seizure
A
focal onset, impaired consciousness, begin as simple partial and progress to impaired consciousness
18
Q
types of partial / focal seizures
A
simple, complex, partial secondarily generalized
19
Q
types of generalizes seizures
A
generalized tonic-clonic (grand mal), absence (petit mal), tonic, atonic, clonic and myoclonic, infantile spasm
20
Q
primary generalized epilepsies
A
age dependent, generalized 2.5-4 Hz bifrontal spikes, polyspikes and slow wave discharge, no structural abnormality, normal intelligence, often genetic component
21
Q
secondarily generalized seizure
A
start local and evolve into tonic-clonic seizures, no genetic component, result of brain disease due to congenital malformation or metabolic defect
22
Q
partial / focal seizure
A
no loss of consciousness, classified by clinical manifestation (motor, sensory, autonomic, psychic), aura (subjective preceding manifestation - is the initial phase of focal seizure) - can lead into altered consciousness
23
Q
convulsive seizures
A
commonly tonic-clonic (grand mal), less commonly pure tonic, pure clonic, clonic-tonic-clonic generalized
24
Q
nonconvulsive seizures
A
brief lapse / absence in consciousness (petit mal), also can include minor motor (brief myoclonic, atonic, tonic)
25
status epileticus
acute, prolonged epileptic crisis - seizure >30 min or repeated seizures for >30 min without recovery, tonic clonic seizures are most concerning, if airway compromised may have brain damage / death from - hypoxia / cardiac arrhythmia / lactic acidosis
26
non-convulsive status epileticus
neuronal damage due to increased metabolic activity is debated, possible ischemic brain damage in elderly
27
tonic - clonic seizures
type of generalized seizure across entire brian (grand mal), aura often precedes, tonic phase - loss of consciousness and tense muscles, clonic phase - muscles contract and relax rapidly causing convulsions
28
myoclonic seizures
more common in 0-14 yrs, brief involuntary twitching of muscles or group of muscles, can be hiccups, often occur after waking up
29
partial seizures
limited to specific area in brain, can include any movement, sensory or auditory symptom, simple - 30-60sec with no loss of consciousness, complex partial -1-2min with aura and automatisms and lack of awareness
30
absence seizures
more common in 0-14 yrs, petit mal, no aura, abrupt onset, brief, prompt recovery, altered consciousness, no extreme muscle effects, may effect learning
31
complex partial seizures
more common 15-65 yrs, effect larger area of brain than simple partial seizures, can't interact, no memory of event, altered consciousness
32
dysprosody
can speak, abnormal expression of emotion/tone/inflection/emphasis, inability to interpret and comprehend emotion/tone in speech, caused by lesion to right (nondominant) hem opposite Broca's area
33
frontal lobe lesion
problems with executive function - like mood, orientation, concentration, appropriate social behavior
34
Glasgow Coma Scale
use if pt unresponsive in ER,
35
suicide
males - more violent and successful, females - less violent and successful
36
attention deficit hyperactivity disorder
developmental, three traits - attention prob / hyperactive / impulsiveness occurring together, starts before 7 yrs, 5-10% school kids, decreases into adulthood, prob kids misdiagnosed, 6 attention or 6 hyperactive symptoms present for 6 mnths in more than one setting and causing difficulties, parent / teacher questionnaire, IQ / psych test / evaluation
37
attention deficit hyperactivity disorder
deficient NE and DA activity in pathways - Tx raising DA / NE reduces symptoms
38
ADHD NE pathway
locus coeruleus -> frontal and limbic cortex, focus, attention, working memory
39
ADHD DA pathway - mesocortical
tegmentum -> frontal and limbic cortex, mediates cognitive functions
40
ADHD DA pathway - nigrostriatal
substantia nigra -> striatum, motor hyperactivity / impulsiveness
41
ADHD DA pathway - mesolimbic
ventral tegmentum -> nucleus accumbens, euphoria (reason for abuse)
42
alzheimer disease (AD)
cortical degeneration, dementia, impaired higher function, altered mood / behavior, progressive, disorientation, memory loss, aphasia, elderly, 40% > 80 yrs, destruction of cholinergic (ACh) neurons in neocortex / amygdala / hippocampus / frontal cortex (from nucleus basalis of Meynert)
43
alzheimer microscopic
neurofibrillary tangles inside neurons, beta amyloid polypeptide plaques
44
neurofibrillary tangles
tau proteins around neuron microtubules, interfere with axonal transport leading to cell death
45
beta amyloid polypeptid plaques
nucleus basalis of meynert neurons over produces, accumulate at synapse, interferes with cholinergic transmission leading to die off of innervated areas
46
alzheimer progression
memory problems - neuronal loss in nucleus basalis of meynert, 3 years - cell damage / loss spreads (diagnosis and loss of independence), 3-6 years - neocortex heavy cell death, 3 years - pt death
47
metastatic brain tumors
70% of CNS tumors, 25% 0f tumors spread to the brain, lung, breast, kidney, liver, and melanoma primary cancers (determines tx)
48
primary brain tumors
30% of brain tumors, adults, giloblastoma multiforme and meningioma
49
metastasis brain tumors
well circumscribed, multiple sites, junction of gray and white matter (meningeal carcinomatosis)
50
primary brain tumors
poorly circumscribed (infiltrating fingers), single, location by type
51
CNS tumors in children
second most common neoplasm in children, medulloblastoma and astrocytoma
52
typical CNS tumor tx
surgery first if possible, followed by adjuvant chemo or radiation following to remove residual cancer cells
53
brain tumor locations
kids - 70% in posterior fossa, adults - 70% supratentorial (hemispheric)
54
WHO grade 1
brain tumor with low proliferative potential, cured with surgery alone
55
WHO grade 2
brain tumor that is infiltrative but low proliferative activity, fingers but slow growing, 5 year survival
56
WHO grade 3
brain tumor that is malignant, showing nuclear atypia and mitotic activity - looks disorganized, 2-3 year survival
57
WHO grade 4
brain tumor that is malignant, mitotically active, necrosis prone in center, rapid pre and post operative progression, elderly GBM not more than 1 year
58
brain tumor grading
graded with localizing / imaging, further graded during surgery, affected by age / location / performance / radiological features / extent of resection / proliferation / genetic alterations (no blood / urine markers)
59
radiation for brain tumors
breaks DNA in tumor cell, many breaks = cell death, some may be resistant to radiation
60
gliomas / astrocytomas
astrocytes / oligodendrocytes / ependymal cells, high grade = fatal, infiltrative
61
glioblastoma multiforma (GBM)
highest grade astrocytoma, most malignant
62
glioma symtoms
headache, seizures, memory loss, changes in behavior
63
pilocytic astrocytoma
grade I astrocytoma, benign, low proliferative, children (0-19), posterior fossa, cerebellum, good prognosis, cystic, long hair-like bipolar cells, rosenthal fibers (corkscrew - eosinophilic - made GFAP proteins), biphasic - loose/inactive and dense/active cell areas, hole = edema
64
pilocytic astrocytoma genetics
targeted therapy to the BRAF (RAF) mutation that prevents the formation of nuclear transcription factors (BRAF also common in melanoma)
65
diffuse astrocytoma
grade II astrocytoma, low proliferative, infiltrative, turns into secondary gliobastoma (bad), slow progress, becomes anaplastic, surgery followed by radiation (for slow cells), 20-39 yrs old
66
diffuse astrocytoma microscope
more cells, mostly astrocytes with round nuclei
67
fibrillary astrocytoma
fibers running through it, many astrocytes with round nuclei
68
gemistocytic astrocytoma
many large astrocytes filled with GFAP protein, astrocytoma variant
69
genetic mutations and astrocytic gliomas
diffuse astroctyoma with P53 mutation worse survival rate, oligodendroglioma with 1p/19q loss mutation better survival
70
anaplastic astrocytoma
grade III, more cellular regions / pleomorphism / mitoses, cells filled with GFAP fibers, cells in undifferentiated state, enlarged nuclei
71
GFAP
glial fibrillary acidic proteins, intermediate filament in mature astroctye, modulates motility and shape, activated after injury causing astrogliosis
72
glioblastoma
grade IV astrocytoma, varied appearance, necrosis, vascular proliferation
73
primary glioblastoma
most common primary brain tumor, adults 45-75 yrs, 10 mnth survival, butterfly glioma crosses midline, pseudopalisading necrosis
74
glioblastoma mutliforme GBM
slow progessing neuro deficit (motor weakness), headache, ICP, headache, nausea, vomting, cognitive impairment, seizures, 45-75 yrs
75
glioblastoma butterfly lesion
travels across corpus callosum
76
pseudopalisading nuclei
look stacked, not in location that normally has stacked nuclei, found in glioblastoma
77
secondary glioblastoma
can arise from diffuse astrocytoma or anaplastic astrocytoma, commonly from precursor cells with IDH1/2 mutation and TP53 mutation
78
oligodendroglioma
less common, adults, seizures, 5-10 yr survival, 1p/19q deletion improves survival, circumscribed, heminspheric, round nuclie with cytoplasmic halos (fried egg), delicate capillaries, calcified
79
ependymoma
line vesciles in CNS, children, fourth ventricle, less common adults in spine, slow growing, 4 yr survival, CSF dissemination, solid or papillary, round nuclei, dense fibrillary, canals, pseudorosettes, rosettes, try to make little ventricles
80
rosettes
canals/lumen surrounded by cells in ependymoma
81
vascular pseudorosettes
vessels surrounded by fibers in ependymoma
82
Homer-Wright rosette
cells surrounding nerupil, in medulloblastoma and primitive neuroectodermal tumor (PNET)
83
Flexner - Wintersteiner rosette
retinoblastoma, cells around cytoplasmic extensions of tumor
84
medulloblastoma
primitive neurons, children, cerebellum, very radiosensitive, i(17q) mutation has poor prognosis, well circumscribed, small, dark , elongated, anaplastic, Homer-Wright rosettes, pseudorosettes, headache, AM vomiting, back pain, motion problems, 0-10 yrs esp males
85
i(17)(q10) mutation
very bad prognosis in medulloblastoma, isochrome 17 i(17) part of chromosome breaks off / flips / reattaches at q10
86
primary brain lymphoma
rare, immunosuppressed, detectable in CSF, aggressive, responds poorly to chemo, large, B cell lymphoma (EBV), multiple nodules, necrotic foci, periventricular, hard to tell from trophasomes in HIV
87
ring enhancing lesion
multiple, cerebral and basal, from toxoplasmosis, immunocrompromised
88
meningioma
second most common primary brain tumor, benign, arachnoid cells, slow growing, surgery, attached to dura, compresses brain, syncytial pattern (cells in circular bundles), psammoma bodies (calcium deposits)
89
schwannoma
third most common brain tumor, CN VII at cerebellopontine angle, hearing loss, tinnitus, good prognosis, surgery, normal palisading, hypercellular and hypocellular areas
90
retinoblastoma
sporadic are unilateral, familial are bilateral and associated with osteosarcoma, Flexner-Wintersteiner rosettes
91
craniopharyngioma
odontogenic epithelium, children - young adults, calcified, benign, recurring, compression of optic chiasm - vision problems
92
myxopapillary variant of ependymoma
adults, in spinal cord (filum terminale), myxoid mass, mucinous/myxoid degeneration, well circumscribed, surgery
93
depression
sadness, pessimism, worry, agitation, withdrawal, somatic concerns, sleep / eat changes, mental slowing - 15% suicide, 4th most common complaint in primary care, 1/10 has it, medical care over utilizers
94
mania
high energy, euphoria, rapid speech, racing thoughts, decreased sleep, hypersexual, excessive goal behavior
95
unipolar depression
once, recurrent separated by euthymia
96
bipolar disorder
mood alternation between depression and mania, may be separated by euthymia, cycle rapidly, occur concurrently
97
amine hypothesis of depression
insensitive amine receptors or deficient amine synthesis / storage / release, amines = norepinephrine and serotonin
98
amine hypothesis of mania
excess amines (norepinephrine, serotonin)
99
problem with amine hypothesis of mood disorders
mismatch between time course, neurochemical effects 1-2 days, clinical improvement 10-21 days
100
psychosis
psychiatric illness, DA levels increased, locus in limbic system, tx block DA receptors, tx causes parkinsonism
101
parkinsonism
neurologic illness, DA levels decreased, locus in striatum, tx increase DA levels, tx causes psychosis
102
psychosis
psychiatric illness, impaired behavior / coherent thought / comprehension of reality, delusions and hallucinations, includes schizo / delirium / dementia / bipolar / psychotic depression / drug induced
103
schizophrenia positive symptoms
delusions, hallucinations (auditory), disorganized throught / speech, disorganized behavior, catatonic - gained functions
104
schizophrenia negative symptoms
lack of emotion / interest in life / flattening / alogia (inability to speak) / social skills - loss of functions
105
schizophrenia cognitive symptoms
disorganized thought, slow thought, difficulty understanding, poor concentration, poor memory, difficulty expressing/integrating thought
106
dopamine hypothesis of schizophrenia
caused by increased DA, increased D2 receptor activity causes psychoses - proof: amphetamines increase DA and cause psychosis, first gen anti-psychotics block DA receptors as seen to work, weakness - DA levels only seem to be related to positive schizoprenia symptoms
107
four DA pathways in the brain
1. mesolimbic, 2. mesocortical, 3. nigrostriatal, 4. tuberoinfundibular
108
mesolimbic DA pathway
tegmentum -> nucleus accumbens, mediates positive symptoms of schizophrenia, block DA D2 receptors and symptoms decrease, drugs that increase DA (amphetamine / cocaine) cause positive symptoms in this pathway
109
mesocortical DA pathway
tegmentum -> frontal and limbic cortex, mediates negative symptoms of schizophrenia, decreased DA levels produces / worsens negative symptoms, why neg symptoms are worsened by antipsychotics that block DA receptors - second gen antipsychotics affect both DA and 5HT receptors and are better at tx for neg symptoms
110
nigrostriatal DA pathway
substantia nigra -> basal nuclei, regulates posture and voluntary movement, first generation antipsychotics block DA receptors producing parkinsonism, second gen antipsychotics less likely to produce parkinsonism
111
tuberinfundibular DA pathway
hypothalamus -> anterior pituitary, DA inhibits prolactin release, first gen antipsychotic females may experience galactorrhea / amenorrhea / sexual dysfunction
112
at risk of abusing prescription drugs
doctors, nurses, dentists, PAs, vets, pharmacists, prof pts
113
abused prescription drugs
opiods, anxiolytic-sedative-hypnotics, CNS stimulants
114
abused opioids
morphine, codeine, heroin, oxycodone, hydrocodone, tx for pain, temporary bliss with indifference to environment
115
abused anxiolytic-sedative-hypnotics
more benzodiazepines (diazepam, alprazolam) than barbiturates, tx for anxiety and insomnia, produces disinhibition euphoria - white collar "alcoholsim"
116
CNS stimulants
methylxanthine (caffeine), andrenomimetics (dextroamphetamine, methamphetamine, methylphenidate - ritalin), tx for narcolepsy and ADHD, increases wakefulness / attentiveness / performance - used in college
117
other drugs of abuse
cocaine, phencyclidine, LSD, MDMA, ketamine, flunitrazepam, ethanol, nicotine, caffeine
118
psychoactive drugs
alter behavior, seek drugs that alter consciousness in pleasurable way, society determines what is drug abuse
119
tolerance
decreased effect of drug, increased dose needed
120
cross tolerance
tolerance to drugs in same group
121
opioids tolerance
rapid - analgesia; slow - miosis, constipation
122
barbiturates / benzodiazepines
fast - sleep; slow - antiseizure, lethal
123
psychological dependence
feel a sense of doom if can't get a drug
124
physical dependence
withdrawal
125
addiction
not same as physical dependence, addiction becomes central to life / behaviors
126
drug misuse
drug within medical context, ill advised patterns of prescribing
127
drug abuse
use drugs for psychic effects, non-medical, disapproval from society
128
type I drug abuse
pt has hx of drug abuse
129
type II drug abuse
takes drug for medical reason, becomes addicted, rare if not a myth - esp if meds properly managed
130
prescription drug abuse rates
rising, 60% of drug related ER visits, 70% of drug related deaths from prescription drugs, 30% of street drugs
131
sources of street prescription drugs
clandestine labs, pharmacy burglary, diversion from health professionals
132
should be aware or Rx drug abuse because...
social responsibility (know drug action and uses), professional responsibility (right dose to right pt for right reason), personal responsibility (protect medical practice)
133
MN physician Rx abuse discipline
rx to pt with known addiction, unmonitored opioid rx, rx with no physical exam, rx with known drug interaction, rx in known contraindications
134
type of doctor Rx drug abusers target
dishonest, disabled, deceived, dated
135
protect Rx pad
safe storage, use one at a time, numbered consecutively, do not sign in advance, write in ink, write out amount of meds, no notes/ memos, do not leave unattended
136
drug seeking behaviors
ask for specific meds, request more, claim allergy and lack of efficacy, evasive answers, traveling through town, no primary doc, lost prescription, late afternoon apt on Friday
137
Rx drug abuser scams
altered script by adding zero, sick grandpa with allergy to certain meds, accomplice in the health care office, pt posed as doctor to pharmacy
138
when in doubt...
ask for photo ID, verify DEA number on a script, hang a notice in your office, do not confuse drug seeking with unresolved pain
139
brain injury
leading cause of death/disability ages 1-44 yrs
140
primary brain injury
happens in first 4 hrs, leads to secondary brain injury which the part you want to prevent
141
coma
sustained altered consciousness, pathologic (unless iatrogenic)
142
Glasgow coma scale
14
143
Monro-Kellie hypothesis
19
144
CT scan
CT is like 360 x-ray that measures density in Houndsfield unit (fluid 0HU, air -1000HU, bone 1000HU), normal brain 40-70HU, image of choice for brain injury, head CT takes 8 sec, good at looking for blood to decide if there is a pressure problem
145
normal on CT
calcified choroid plexus / pineal gland
146
pressure problem in skull
must determine, if present = emergency, CT scan, GCS, too much blood / brain / CSF - only so much blood and CSF can be subtracted, then brain starts to be damaged (must do something before this happens) - brain will herniate into foramen magnum
147
most common subarachnoid hemorage
trauma by far, then nontrauma aneurysm - happens in evening - those that survive have clotted off
148
fully absructed hyprocephalus
dead in 6 hrs, make 18 ml CSF / hr
149
bad on CT
midline shift, whiter hyperdense areas (acute blood) or darker hypodense (chronic blood), gyri and sulci compressed and not showing
150
acute blood on CT
hyperdense - looks white
151
chronic blood on CT
hypodense - looks dark
152
change the rules for brain swelling
take away some bone and leave off, allows brain to swell, done especially with gun shot wounds
153
subdural hemorrhage
fuzzy edges, follows curve of the skull
154
epidural hematoma
lens shaped mass, edges demarcated, venous bleed (survive), arterial bleed (don't live)
155
hydrocephalus from blood filled ventricles
shunt out of head, only put in with low GCS
156
cerebrovascular disease
stroke, three mechanisms thrombosis (clot at location)/embolism (moving object - usually clot)/hemorrhage (can form mass or go into subarachnoid space), lack of blood or ruptured vessel are two main mechanisms, acute focal neurological loss, 3rd cause of death in US
157
global cerebral ischemia
hypotension, mild - transient confusion, severe - persistent vegitative state/brain death, can last 4min without damage, watershed infarcts - temporary hypotension causes loss of blood to area where major vessel branches end - thin gray matter, loss of brain mass
158
global cerebral ischemia histology
first day - red neurons/neutrophils, then - necrosis/macrophages/vessel proliferation/gliosis, after weeks - loss of necrotic tissue leaving open space
159
areas susceptible to hypoxia
watershed areas (where branches of two larger arteries meet), lamina (where areas of cortex meet)
160
watershed infarcts
edges of two major arteries, looks like hypodense dark diffuse area on CT
161
focal cerebral ischemia
obstructed blood flow to one area of brain, two types - ischemic and hemorrhagic
162
ischemic focal infarct
thrombi develops in vessel, from atherosclerotic plaque, look pale, broader circular area affected
163
hemorrhagic infarct
look red, from emboli (moves) and reperfusion injury from weakened vessel, emboli often from heart esp with atrial fibrillation / patent foramen ovale, more focal area affected
164
transient ischemic attacks
temporary with no signs on imaging, are harbingers of ischemic infarct later
165
thrombosis causes
atherosclorsis, carotid bifurcation/middle cerebral artery origin/ends of basilar artery, leads to ischemic infarction
166
embolism causes
blood clot, heart/carotid/marrow/fat/tumor, middle cerebral artery branch points, lead to hemorrhagic infarction
167
ischemic infarct gross
days - white, swollen, 10 days - gelatinous, outlines visible, weeks - liquefaction and cavitation
168
hemorrhagic infarct gross changes
punctate hemorrhages or big hematoma, resolution and cavitation
169
focal infarct micro changes
hours - days: red neurons, edema, swelling, neutrophils, macrophages; weeks - gliosis, more macrophages, dense gliosis, new capillaries, ischemic and hemorrhagic infarcts look microscopically the same but hemorrhagic has extravasated blood
170
lacunar infarct
causes lacunar infarcts in deep cerebral vessels (basal ganglia, deep white matter, brainstem), tiny infarct with tissue loss/macrophages/gliosis, can be clinically silent or cause severe impairment, caused by arteriolar sclerosis that occludes vessel
171
slit hemorrhage
hypertension ruptures little vessels, little hemorrhages, leave brown slit-like cavity, hemosiderin-laden/lipid laden macrophages and gliosis
172
acute hypertensive encephalopathy
acute malignant hypertension, diffuse effect - confusion / convulsion / coma, increasing ICP, swollen brain with petechia and fibrinoid necrosis on arterioles
173
hypertensive cerebrovascular disease
lacunar infarct, slit hemorrhage, acute hypertensive encephalopathy
174
intracranial hemorrhage
anywhere in/around brain, subdural/epidural hemorrhage is usually from trauma, hemorrhage in parenchyma / subarachnoid space usually from cerebrovascular disease
175
parenchymal hemorrhage
around 60, high mortality, commonly rupture of small intraparenchymal vessel, ganglioic or cortico lobar, commonly caused by hypertension
176
hypertension as cause of parenchymal hemorrhage
HT causes atherosclorsis, hyaline arteriolosclerosis, frank necrosis, weakens vessel walls, sometimes time aneurysms (Charcot-Bouchard microaneurysm)
177
subarachnoid hemorrhage
rupture of berry aneurysm common, other causes - rupture of intracranial hemorrhage into subarachnoid space, coagulopathy, vascular malformation, tumors, traumatic hematoma extension
178
berry aneurysm
mostly sporadic, risks - smoking and hypertension, grow slowly, >1cm have 50% risk of bleed / year, common at arterial branch points, thin sac, high mortality with rupture
179
subarachnoid hemorrhage clinical findings
severe headache (worst ever), loss of consciousness in minutes, death in 25-50%, regain consciousness if survive, risk of vasospastic injury or communicating hydrocephalus do to blockage near CSF resorption location
180
alzheimer disease
degenerative disease of cortex neurons, dementia, gross atrophy of brain, microscopic plaques and tangles, 3-20 yr prognosis
181
alzheimer symptoms
most common cause of dementia in elderly, 40% at 85 yrs, early - forgetful in higher level functions/mood/behavior, then - disorientation/memory loss/ motor skill loss, 5-10 year - profound disability/mute/immobile, death common from infection (pneumonia)
182
alzheimer progression - parts of the brain
affected first - hippocampus (memory) and language (temporal/frontal cortex), later - entire cortex from front to back with disease progression (personality/mood changes, then motor changes)
183
neuritic plaques - alzheimer
dilated, tortuous neurites around amyloid core, contain beta amyloid
184
neurofibrillary tangles - alzheimer
bundles of filament in neuron cytoplasm, made of tau, MAP2, and ubiquitin
185
other microscopic changes - alzheimer
neuronal loss, gliosis, cerebral amyloid angiopathy, granulovasuolar degeneration, Hirano bodies collections of actin
186
alzheimer pathogensis
deposition of Abeta peptides from abnormal processing of amyloid precursor protein, Abeta accumulates making amyloid aggregate that are neurotoxic and inflammatory, tau accumulation in tangles seems to be secondary (other dementia diseases have tau deposition on microtubules)
187
normal amyloid precursor protein cleavage
usually cleaved into three parts, abnormal secretase enzymes, Abeta portion of cleavage forms aggregate
188
pick disease
rare, distinct, progressive dementia, frontal lobe signs (personality change) and temporal lobe signs (language problems), severe atrophy in both lobes, neuronal loss / swelling, pick bodies with tau protein in neuronal cytoplasm - does not progress to occipital lobe
189
parkinson
degeneration of substantia nigra neurons, tremor, rigidity, bradykinesia, atrophy of substantia nigra, Lewy bodies in cells, slightly shortened life
190
parkinson symptoms
facial mask, stooped posture, slowed voluntary movement, festinating gait, rigidity, pill-rolling tremor, responds to L-DOPA, autonomic/cognitive dysfunction, some dementia, L-DOPA tx symptoms but does not slow disease
191
parkinson morphology
palor of substantia nigra, loss of pigmented neurons in substantia nigra, lewy bodies in cells in nucleus of Meynert, neuronal loss
192
parkinson pathogenesis
5 associated genes, unknown mechanism, possibly alpha-synuclein (in lewy bodies), degeneration of DA neurons
193
deep brain stimulation with parkison / severe depression
electrode in brain, stops inhibition of thalamus allowing motor movement, wear pace maker under the skin
194
amyotrophic lateral sclerosis (ALS - lough gerigs disease)
degeneration of motor neurons, rapid progressing weakness/spasticity/dysphagia, sensory and cognitive function intact, death within 2-3 years from resp compromise
195
ALS clinical
early - hand weakness, arm/leg spacticity, twitch, slurred speech; then - atrophy, fasciculations, creeping paralysis; later - resp muscles effected and infection
196
progressive muscular atrophy
lower motor neurons only
197
progressive bulbar palsy
upper motor neurons, symptoms around mouth / face, progress faster
198
ALS pathogenesis
superoxide dysmutase mutation in some inherited cases, impaired ubiquitin 2 housekeeping protein in all cases, misfolded / accumulated proteins?
199
ALS morphology
thin anterior roots of spinal cord, anterior horn neurons reduced, skeletal muscle atrophy, degeneration of corticospinal tract
200
continuum of cognition
normal aging, mild cognitive impairment, dementia
201
alzheimer pathophysiological cascade
age/gentics + cerebrovascular risks -> Abeta amyloid accumulation -> synpatic dysfunction / glial activation / tangle formation / neuronal death -> cognitive decline
202
alzheimer course
preclinical - amyloid beta accumulation / synpatic dysfunction / tau neuronal injury; mild cognitive decline - tau neuronal injury / brain structures affected / cognition effected; dementia - cognition / clinical function; preclinical almost matches normal aging decline until mild cognitive decline presents
203
biggest risk factor for alzheimer with hallucinations/delusions
isolation
204
gioblastoma multiforme microscopic
hyperchromatic (mitotic), pleomorphic, psuedopallisading around necrosis, vascular proliferation, anaplastic sheets
205
gliobastoma multiforme tx course
resection, radiation, temozolomide chemo if candidate and O-methylguanine methyltransferase gene is methylated
206
glioblastoma multiform
psuedopalisading cells around necrotic tissue, anaplastic cells, hyperplastic vessels, 60-70 yrs, 12 mnth survival, grade 4 by definition, grow fast, butterfly lesion
207
glioblastoma multiform symptoms
seizures, headache (positional), neuro deficits - weakness, dysphagia, dyspraxia, ataxia, increased ICP, CN problems
208
tumor vs necrotic abscess vs infectious abscess on MRI
if infectious - shows in labs results too, abcess likely better demarcated than infiltrative tumor, necrosis darker on T1 MRI - know true difference by biopsy
