1
Q
what are the general clinical feature of CNS tumors
A
Clinical features: focal neurological deficit (usually due to compression), seizures (usually with cerebral cortex), general neuro sx (HA, AMS), increased ICP
Increased ICP tends to be due to: growth of neoplasms, peritumoral edema, secondary changes to neoplasm (cysts, hemorrhage), or obstruction of CSF pathway àbrain herniation
2
Q
Primary vs Metastatic
regarding CNS tumors
A
- Metastatic (poor prognosis)
- Etiology: Metastatic tumors present as multiple, well-circumscribed lesions usually from lung, breast, or kidney tumors
- Site: cerebellum, cerebrum, vertebral bodies with compression of spinal cord
- Micro: resembles original tissue
3
Q
Adult vs Children
CNS tumors
A
Adults usually get supratentorial tumors while children get infratentorial tumors
4
Q
Craniopharyngioma
epidemiology, locations, micro, gross, prognosis, tx
A
- Epidemiology: children, but can also be seen in adults
- Location: suprasellar (origin from Rathke’s pouch) –> can cause bitemporal hemianopsia
- Micro: crystals found in “motor oil” and calcifications (see pic)
- Gross: well-defined cystic mass; may be calcified
- Prognosis: benign; high ten-year survival if small and excised
5
Q
Neurofibroma
epidemiology, locations, micro, gross, prognosis, tx
A
- Etiology: genetic (NF1 mutation) or sporadic mutations
- Location: cutaneous/visceral nerves, spinal roots
- Micro: S100 positive Schwann cells, NFP-positive axons present; spindle cells with wavy collagen (see pic)
6
Q
Schwannoma (malignant tumor of Schwann cells)
epidemiology, locations, micro, gross, prognosis, tx
A
- Epidemiology: adult
- Location: anywhere Schwann cells are present; classically at the cerebellar-pontine angle, peripheral nerves, CN VIII (vestibular Schwannoma)
- Micro: S100 positive, contain compact areas (Antoni A – see star) and loose areas (Antoni B – see arrow), palisading growth pattern (Verocray bodies) is typical of Antoni A
- Gross: well-defined, compressing surrounding tissue; if bilateral –> NF-2
- Prognosis: good, treated with surgery
7
Q
Meningioma
epidemiology, locations, micro, gross, prognosis, tx
A
- Epidemiology: very common tumor in adults
- Location: anywhere where arachnoid cells are found (meninges)
- Micro: proliferation of arachnoid cells; whorling growth (see pic), psammoma bodies
- Gross: well-defined tan-fibrous mass attached to dura –> compressing adjacent CNS tissue
- Prognosis: good prognosis; benign; can be excised
8
Q
Pinealoma
epidemiology, locations, micro, gross, prognosis, tx
A
- Epidemiology: children
- Sx: can cause parinaud syndrome (compression of tectum –> vertical gaze palsy), hydrocephalus, precocious puberty in males (beta-HCG production)
- Micro: looks like testicular seminoma/germ cell tumor
9
Q
Hemangioblastoma
epidemiology, locations, micro, gross, prognosis, tx
A
- Epidemiology: adult; associated with von-Hippel-Lindau syndrome with retinal angiomas
- Location: cerebellum
- Micro: closely arranged thin-walled capillaries; produces EPO –> secondary polycythemia
10
Q
Medulloblastoma
epidemiology, locations, micro, gross, prognosis, tx
A
- Epidemiology: children (common tumor in children)
- Location: cerebellum (esp. vermis)
- Micro: Homer Wright rosettes (see pic - cells surrounding vessel), small blue cells, synapthophysin (yellow) IHC
- Gross: well-defined; may extend into 4thventricle/aqueduct/CSF foramina àhydrocephalus
- Prognosis: highly malignant, but 5 to 10 year survival possible with treatment (surgery/chemo); drop metastasis via CSF to spinal cord possible
11
Q
Ependymoma
epidemiology, locations, micro, gross, prognosis, tx
A
- Epidemiology: children or young adults
- Location: 4thventricle (in children) and caudal end of spinal cord (in young adults)
- Pathophysiology: due to location, may block CSF flow and spread along CSF pathways àhydrocephalus
- Micro: perivascular pseduorosettes (see pic - cells surrounding a vessel), rod-shaped blepharoplasts (basal ciliary bodies), ependymal canal seen
- Gross: well-defined (note location)
- Prognosis: poor if in ventricle; good if caudal end of spinal cord
- Treatment: gross total resection with possible radiotherapy
12
Q
Oligodendroglioma
epidemiology, locations, micro, gross, prognosis, tx
A
- Epidemiology: adult
- Etiology: deletions of 1p and 19q chromosomes
- Location: frontal lobes
- Micro: round nuclei, clearing of cytoplasm (see pic – fried egg)
- Gross: calcified circumscribed tumor of white matter
- Prognosis: favorable if treated (mean survival: ten years)
- Treatment: surgical excision with or without temozolomide and PCV (procarbazine, lomustine, vinicristine)
13
Q
Glioblastoma Astrocytoma (Grade IV)
epidemiology, locations, micro, gross, prognosis, tx
A
- Epidemiology: 50s to 70s
- Location: cerebral hemispheres
- Micro: pseudo-palisading pleomoprhic tumor cells, mitotic figures prevalent, poorly differentiated, GFAP-positive, vascular proliferation (see pic)
- Gross: ill-defined borders; necrosis, hemorrhage; not homogenous, crosses corpus callousàbutterfly lesion
- Prognosis: poor (12-month survival); if progression from lower grade àbetter prognosis
14
Q
Anaplastic Astrocytoma (Grade III)
epidemiology, locations, micro, gross, prognosis, tx
A
- Epidemiology: 40s to 60s
- Location: cerebral hemispheres
- Micro: highly infiltrative, poorly differentiated, increased mitotic activity (see pic), no vascular proliferation
- Gross: ill-defined edges on MRI
- Prognosis: mean survival about 3 years
15
Q
Diffuse Astrocytoma (Grade II)
epidemiology, locations, micro, gross, prognosis, tx
A
- Epidemiology: 30s to 40s
Location: cerebral hemispheres
Micro highly infiltrative astrocytic cells (see pic - small dark cells diffusely), no mitotic activity, no vascular proliferation/necrosis
Gross: ill-defined edges on MRI
Prognosis: usually progress to anaplastic astrocytoma or glioblastoma, 6-8 year survival
16
Q
Pilocytic Astrocytoma
epidemiology, locations, micro, gross, prognosis, tx
A
- Epidemiology: most common glial neoplasm in children
- Location: cerebellum and optic nerve pathway/hypothalamus
- Micro: Rosenthal fibers (see pic - red corkscrew fibers), biphasic pattern of density, GFAP-positive, eosinophilic (granular bodies found)
- Gross: on imaging, cystic lesion with mural nodule (white dot with black around it)
- Prognosis: benign; excellent prognosis with total excision
- Treatment: surgical excision
17
Q
A
Pilocytic Astrocytoma (Grade I)
18
Q
A
Diffuse Astrocytoma (Grade II)
19
Q
A
Anaplastic Astrocytoma (Grade III)
20
Q
A
Glioblastoma Astrocytoma
21
Q
A
Oligodendroglioma
22
Q
A
Ependymoma
23
Q
A
Medulloblastoma
24
Q
A
Meningioma
25
Schwannoma
26
Neurofibroma
27
Craniopharyngioma
28
Myasthenia gravis
epidemiology, pathophys
* Epidemiology: women (more common: 20s to 40s), men (40s to 60s); first degree relatives have a higher incidence
* Pathophysiology: auto-antibodies to post-synaptic Ach receptors → destruction of Ach receptors → weakness of muscles
29
Myasthenia gravis
sx, dx, tx
* Signs/sx: ptosis → frontalis sign (wrinkling of forehead), diplopia, dysarthria, dysphagia, weakness (improves with rest; worsens with activity), fatigability, nasal (weakness of soft palate), slurred speech (weakness of tongue, lips, and faces; dropped head appearance
* Associated with thymoma and thymic hyperplasia; ocular involvement is a must
* NO pupillary dysfunction, cognition, autonomics, or sensory deficits
* Diagnosis: Ice test (improves ptosis), lab studies (for Ab), Edrophonium/Tensilon (acetylcholinesterase inhibitor), electrodiagnostic study, imaging to exclude thymoma due to hyperthyroidism (can cause ptosis)
* Treatment: pyridostigmine (AchE inhibitor), prednisone, IVIG, plasmapharesis
30
Lambert-Eaton Myasthenic Syndrome (LEMS)
* Pathophysiology: autoantibodies to presynaptic Ca channels → decreased Ach release
* Associated with: paraneoplastic syndrome (i.e. small cell lung cancer)
* Signs/sx: proximal muscle weakness (improves with use → increased availability of ACh), autonomic sx (dry mouth, impotence)
* Eyes are spared
31
Botulism
* Etiology: Clostridium botulinum
* Pathophysiology: Toxin cleaves SNARE proteins → prevents release of Ach → paralysis
* Signs/sx: dilated pupils, muscle weakness
* Diagnosis: EMG (nerve stimulation → increase in muscle fiber contraction)
32
Polymyositis
sx,dx,tx
* Signs/sx: proximal muscle weakness, speech and swallowing dysfunction
* NO sensory loss, skin involvement
* Diagnosis (autoimmune): increased CK, EMG shows myopathic features, + ANA, +anti-Jo-1, +anti-SRP, +anti-MI-2 antibodies
* Pathology (see pic): endomysial inflammation with CD8+ T-cells;
* Treatment: steroids (prednisone) with chronic immunosuppressant therapy (methotrexate)
33
Dermatomyositis
sx, dx, tx
* Signs/sx: proximal muscle weakness, rash on upper eyelids (heliotrope rash), malar rash, red papules on elbows/knuckles/knees (Gottron papules)
* Diagnosis (autoimmune): increased CK, + ANA, +anti-Jo-1, +anti-SRP, +anti-MI-2 ABs
* Pathology (see pic): perimysial inflammation (CD4+ T-cells) with perifasicular atrophy
* Treatment: steroids (prednisone) with chronic immunosuppressant therapy (methotrexate)
34
Inclusion Body Myositis
pathology
Pathology: rimmed vacuoles
35
Duchenne Dystrophy
epidemiology, etiology, pathophys
* Epidemiology: males (at birth)
* Etiology:X-linked frameshift mutation of dystrophin
* Pathophysiology: deficient dystrophin → lack of binding of intracellular cytoskeleton to transmembrane proteins (alpha-beta dystroglycan) in plasma membrane of muscle → weak connections to extracellular matrix → myonecrosis → muscle weakness
36
Duchenne Dystrophy
sx,dx,tx
* Signs/sx: delayed milestones, waddling gait, enlarged muscles (pseudohypertrophy: fatty depositions), proximal LE weakness weaker than UE, enlarged tongue, scoliosis
* Other systems: EKG abnormalities/CHF, gastric dilation, intellectual dysfunction
* Diagnosis: Gower’s sign (standing up from kneed position using arms)
* Labs: increased CK (50-100x), aldolase increased
* Electromyography
* Muscle biopsy: shows type I predominance, fibro-fatty replacement
* Dystrophin analysis via western blot
* Treatment: Eteplirsen (Exondys 51) injection, Steroids
37
Becker Dystrophy
etiology,sx,dx
* Etiology: x-linked non-frameshift mutations of dystrophin → truncated protein → see above
* Signs/sx: similar to DMD, but less severe; survival into 40s to 50s
* Diagnosis: same as DMD
38
Myotonic Dystrophy
etiology,pathophys
* Etiology: AD inheritance of CTG trinucleotide expansion of DMPK gene on 19q13
* More repeats = worse disease (anticipation=increased CTG repeats in successive generations)
* Pathophysiology: Mutation of DMPK gene → abnormal expression of myotonin protein kinase → myotonia (delayed muscle relaxation after contraction)
39
Myotonic Dystrophy
sx,dx,tx
* Signs/sx: myotonia, muscle wasting/weakness, cataracts, cardiac arrhythmias, dysarthria, swallowing difficulty
* Facial features: long face, temporo-mandibular wasting, ptosis, frontal balding, atrophy of SCM
* Endocrine abnormalities: diabetes, gynecomastia, testicular atrophy
* Diagnosis:increased CK, EMG (myotonic discharges – dive bomber), muscle biopsy (type 1 fiber atrophy, increased inernal nuclei – see pic)
* Treatment
40
Polymyositis
41
Dermatomyositis
42
Inclusion Body Myositis
43
Myotonic Dystrophy (most common dystrophy)
44
Peripheral Nerve Disease – General
mononeuropathy, mononeuropathy multiplex, polyneuropathy
Mononeuropathy: carpal tunnel syndrome, ulnar nerve neuropathy, peroneal neuropathy,
Mononeuropathy multiplex: at least two different regions with asymmetric nerve deficits
Polyneuropathy: distal, symmetric involvement of nerves in feet\>hand in a gradual manner (i.e. diabetes, alcohol, etc)
45
Carpal Tunnel Syndrome
etiology, sx
* Etiology: entrapment of the median nerve at the wrist
* Associated with: repetitive use of wrist (keyboard/cellphone), RA, pregnancy
* Signs/sx: numbness/sensory loss in median distribution (distal to thenar region, but not thenar region itself – thumb/index finger), atrophy of thenar eminence, weakness/atrophy of abductor pollicis brevis (abducts thumb)
* Sensory loss spared in thenar region due to it being innervated by palmar cutaneous branch of the median nerve (branches before carpal tunnel)
* LOAF muscles: Lumbricals 1 and 2, Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis
46
Carpal Tunnel Syndrome
dx,tx
* Diagnosis: Tinel’s sign (percussion to reproduce tingling), Phalen’s (praying stance), EMG/NCV
* EMG/NCV: indicated prolonged sensory and motor latency (decreased conduction velocity seen in median nerve)
* Treatment: splints at nighttime (avoid flexion of wrist), steroid injection (outside of tunnel), surgery to open tunnel
47
Ulnar Neuropathy
etiology,sx
* Etiology: entrapment across the cubital tunnel or at the Guyon canal (wrist)
* Signs/sx: numbness/sensory loss in ulnar distribution (medial two fingers), and weakness of hand intrinsic muscles (interossei muscles, hypothenar eminence, lumbricals 3 and 4), elbow pain
* In Guyon canal entrapment: sensory loss spared in dorsal surface of medial hand due to it being innervated by dorsal ulnar cutaneous nerve (branches at forearm)
* In cubital tunnel entrapment: both dorsal and palmar surfaces are lost
48
Ulnar Neuropathy
dx,tx
* Diagnosis: subluxation of nerve across elbow segment (risk factor), Tinnel at elbow, EMG/NCV
* Measures conductance at wrist, below elbow, and above elbow → determines if Guyon or cubital issue
* Treatment: splinting to avoid pressure on elbow, steroid injection, surgery (outcomes are less favorable)
49
Peroneal Neuropathy
etiology,sx
* Etiology: crossing legs, excessive weight loss (loss of fat pad cushion at fibular head), fibular neck fracture
* Signs/sx: footdrop (lesion of deep fibular n → weakness of tibialis anterior), weak eversion (lesion of superficial fibular n → weakness of peroneus longus)
* Superficial fibular n: dorsum (top) of foot
* Deep fibular n: between first two toes
50
Guillain-Barre Syndrome (AIDP/GBS)
etiology, pathophys, presentation
* Etiology: demyelinating disease that often occurs post viral illness (campylobacter jejuni)
* Pathophysiology: autoimmune destruction of Schwann cells → demyelination of peripheral nerves and motor fibers
* General presentation: acute or subacute weakness developing over hours to weeks
51
Guillain-Barre Syndrome (AIDP/GBS)
sx,dx,tx
* Signs/sx: facial/bulbar weakness (very common), peripheral muscle weakness, respiratory involvement, LMN signs (areflexia, hypotonia, no atrophy), +/- sensory loss, cardiac irregularities, hypotension/hypertension
* Bell’s phenomenon: tendency of eyes to roll up to show sclera when eyes are shut → can help determine if patient is truly trying to close eyes
* Diagnosis:
* CSF: protein increased (may cause papilledema), no increase in WBC (albuminocytologic dissociation)
* EMG (reveals multifocal demyelination): slowing of conduction velocities, absent/prolonged F response
* Treatment: supportive, mechanical ventilation if needed, plasmapheresis/IVIG (attacks ABs), NO steroids
52
Root Disease/Radiculopathy
description,sx,dx
* Description: compression of nerve roots leading to motor and/or sensory loss
* Signs/sx: pain in root distribution, weakness of muscles in associated myotome, sensory loss/numbness (pinprick and light touch) in associated dermatome, hyporeflexia/areflexia
* Diagnosis: MRI of spine
53
Poliomyelitis
etiology, pathophys,sx,dx
* Etiology: polio virus via feco-oral transmission
* Pathophysiology: virus replicates in oropharynx → small intestines → bloodstream → CNS → destruction of cells in anterior horn → LMN deficits
* Werdnig-Hoffman Disease/Spinal Muscular atrophy (autosomal recessive) – “floppy baby”
* Similar destruction of cells of anterior horn → symmetric weakness
* Signs: LMN signs (asymmetric weakness, hypotonia, areflexia, fasciculations), respiratory weakness, signs of infection (fever, malaise, HA)
* Dx: CSF shows increased WBC, slight increase in protein, no change in glucose
54
Amyotrophic Lateral Sclerosis (ALS)
etiology, epidemiologyy, sx,dx,tx
* Etiology: defect in superoxide-dismutase-1 enzyme (some may have genetic incidence)
* Epidemiology: 40s to 60s; often fatal
* Signs/sx: UMN and LMN lesions, asymmetric weakness (tends to present with bulbar weakness), dysarthria, dysphagia, fasiculations of limbs/tongue, atrophy of intrinsic hand muscles
* NO sensory, bladder/bowel, or cognitive deficits
* Diagnosis: EMG (active and chronic denervation changes in 3 or more muscles)
* Treatment: Riluzone, Edavarone
55
Parkinson’s Disease
description, etiology,
* Description: loss of dopaminergic neurons in the substantia nigra of the basal ganglia
* Affects the nigrostriatal pathway of basal ganglia pathway; normally uses dopamine to initiate movement
* Etiology: unknown, MPTP (contaminant in illict drugs causes Parkinsonian sx)
56
Parkinson’s Disease
sx,dx,complications
* Signs/sx (TRAPS): Tremor (resting), Rigidity (cogwheel), Akinesia (bradykinesia/ expressionless face), Postural instability, Shuffling gait
* Diagnosis
* Histology: Lewy bodies
* Complications: early-onset dementia (Lewy-body dementia – dementia w/ hallucinations)
* Lewy-body dementia: Lewy-bodies are found in the cortex
57
Huntington’s Disease
descritpion,etiology,pathphys
* Description: degeneration of GABAnergic neurons in the nucleus of the basal ganglia
* Etiology: AD trinucleotide (CAG) repeat disorder (\> 36 repeats) on chromosome 4 of huntingtin gene
* Anticipation: repeats increase thru generations → disease worsens
* Pathophysiology: increased CAG repeats → increased glutamine in cells → production of glutamate → Glutamate binding to NMAD-r → Glutamate excitotoxicity in neurons → neuronal death in caudate and putamen (increased lateral ventricle) → excess movement
58
Huntington’s Disease
epidemiology, sx,labs,complications
* Epidemiology: ages 20-50
* Signs/sx: chorea, athetosis (slow chorea), dementia
* Labs: increased dopamine, decreased GABA, decreased Ach
* Complications: death within 10 – 20 years
59
Alzheimer’s Disease
descritption,etiology,risk factors, pathophys
* Description: degenerative disease of cortex, common cause of dementia
* Etiology:
* Sporadic form (elderly): ApoE4 (ApoE2 assoc. w/ decreased risk of Alzheimers)
* Early-onset form (younger): assoc. with APP (chromosome 21), presenilin 1/2
* Risk Factors: Down Syndrome
* Pathophysiology: genetic mutation of APP protein → beta cleavage of APP protein → amyloid-beta → forms plaques → disrupts cortical structures
* Alpha cleavage results in normal amyloid protein → no plaque formation
60
Alzheimer’s Disease
sx,complications,dx
* Signs/sx: slow-onset memory loss (short term → long term), loss of motor skills, language deficits, changes in behavior, neurological deficits not til late, hyperreflexia
* Complication: mute and bedridden late in disease, infection, intracranial hemorrhage (Amyloid angiopathy: amyloid deposition onto vessels)
* Diagnosis
* Gross: narrowing of gyri, widening of sulci, big ventricles (aka cerebral atrophy)
* Histology:
* Senile plaques in neurons
* Neurofibrillary tangles (intracellular hyperphosphorylated tau cytoskeleton proteins → correlated with degree of dementia)
* Loss of cholinergic neurons → decreased Ach
61
Pick Disease
description,sx,patho
* Description: degenerative disease of the frontal and temporal and frontal cortex
* Sign/sx: behavioral (behavioral variant) or language (primary progressive aphasia) sx → progressive dementia
* Associated with parkinsonism/ALS
* Pathology: hyperphosphorylated tau protein (Pick bodies) in neurons or ubiquitinated TDP43
62
Vascular Dementia
description,etiology,sx,dx
* Description: multi-focal infarctions → dementia (second most common cause)
* Etiology: HTN, atherosclerosis, vasculitis
* Signs/sx: stepwise decline in cognitive ability with late onset impairment
* Dx: MRI/CT shows cortical/subcortical infarcts
63
Normal Pressure Hydrocephalus
pathophys, etiology,sx,tx
* Pathophysiology: increased CSF → dilated ventricles → dementia
* Etiology: idiopathic
* Signs/sx: triad of urinary incontinence, gait instability, and dementia (wet, wobbly, and wacky)
* Treatment: LP, ventriculoperitoneal shunting
64
Idiopathic Intracranial Hypertension (pseudotumor cerebri)
description, risk factors,sx,dx,tx
* Description: increased ICP with no apparent cause on imaging
* Risk factors: Vit A excess, female, obese, tetracyclines, danazol
* Signs/sx: HA, CN 6 palsy, papilledema, no AMS
* Dx: LP (increased opening pressure, relief of HA)
* Treatment: weight loss, acetazolamide, topiramate, repeat LPs, CSF shunt placement
65
spongiform encephalopathy
description, etiology, pathophys, sx, patho
* Description: rapidly progressive degenerative disease due to prion protein
* Prion protein normally expressed in CNS neurons in an alpha helical configuration
* Etiology: disease can be sporadic, inherited, or transmitted
* Pathophysiology: Prion converted from alpha-helix configuration to beta-pleated formation → pathological proteins convert normal proteins to diseased proteins → cycle of damage to neurons and glial cells → spongy degeneration
* Signs/sx: cortical signs (speech changes, gait changes, memory loss, personality changes, hyperreflexia)
* Pathology: sponginess of cortex sparing white matter (bottom part)
66
explain Crueutzfeldt-Jakob Disease (CJD) and Fetal Familial Insomnia
* Crueutzfeldt-Jakob Disease (CJD)
* Etiology: sporadic
* Variant CJD: related to bovine spongiform encephalopathy (aka Mad Cow Disease)
* Signs/sx: rapidly-progressive dementia with ataxia and startle myoclonus
* Dx: spike wave complexes are found on EEG
* Complications: death within a year
* Fetal Familial Insomnia
* Etiology: inherited
* Signs/sx: insomnia with exaggerated startle response
67
Gray matter in cerebral cortex
Large purple polygonal shaped cells are neuron cell bodies
68
White matter in cerebral cortex
* No neuronal cell bodies found
Many oligodendrocytes (fried-eggs) and astrocytes (spider-appearance)
69
Normal anterior horn cell:
Motor neurons are large multipolar cells with abundant Nissi substance (granular substance around nucleus)
70
which is normal? what process is going on?
Axonal Reaction
Characterized by central chromatolysis: nucleus of cell body neuron expands and is displaced peripherally, dispersion of Nissi substance, destruction of axon cord àaxonal sprouting
71
which is normal? what happened?
Neuronal Degeneration
Reduction in size of neuron due to progressive or degenerative disease (i.e. Alzheimer’s, ALS)
72
whats going on here?
Transsynaptic “transneuronal” atrophy: lesion to presynaptic terminal --\> postsynaptic cell atrophies
73
what is going on this picture?
Eosinophilic neuronal change (acute neuronal injury)
Red staining of neuronal cytoplasm in H&E stain due to hypoxia or ischemia
74
Intraneuronal Accumulations
what is it?
name soe examples?
Intraneuronal accumulations: accumulation of material within the nucleus or cytoplasm of neurons due to:
* Storage diseases (i.e. Tay-Sachs disease)
* Degenerative disease (Lewy bodies in Parkinson’s disease, neurofibrillary tangles and senile plaques in Alzheimer’s)
Viral inclusions (i.e. Negri bodies in rabies, inclusion bodies in CMV/HSV)
75
name what disease for each pic
a. taysachs
b. parkinsons
c. alzheimers
d. rabies
e. alzheimers again...
76
WHAT PROCESS IS GOING ON HERE?
Astrogliosis: pathological lesion or old infarct àincreased astrocyte deposition àcyst or cavity formation
* Ex: Old infract or MS plaques
77
what process is going on here? examples of dieases
Oligodendrocytes/Myelin Alterations: destruction of ologiodendrocytes (loss of fried egg appearance with cytoplasmic extensions) àdestruction of myelin
Examples: MS, PML (pink intranuclear inclusions)
78
disease?
PML
79
what process is going on here?
Microgliosis during acute injury: inflammation and immune response --\> phagocytosis of dead cells and cellular debris by macrophages
Microglia will appear elongated and many macrophages will be seen
80
what process is going on here?
Ependymal alterations: inflammation or infection of the ventricle --\> loss of ependymal cells --\> aqueductal stenosis --\> congenital hydrocephalus
