MEDEX 452: Pathophysiology for Primary Care
Henry Stoll, PA-C
Spinal Cord Defects
Cerebral Edema
Results of Increased Intracranial Pressure (ICP)
Uncal Herniation
Hydrocephalus -- Causes
Hydrocephalus - Ventricular Enlargement
Hydrocephalus - Results
Brain Blood Supply
Common Sites of Atherosclerosis
Common Sources of Emboli
Stroke - Middle Cerebral Artery
Thrombosis - Internal Carotid Artery
Embolic Stroke with Edema
Embolic Stroke with Punctate Hemorrhages
Watershed Infarctions
Liquefactive Necrosis with Cysts
Basal Ganglia Hemorrhage Due to Hypertension
AV Malformation
Berry Aneurysm

Carotid bifurcation aneurysm
Figure 23-9 Relative frequency of common sites of saccular (berry) aneurysms in the circle of Willis.

Downloaded from: St...
Giant Aneurysms
Ruptured PCOM Aneurysm
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage
Cerebral contusions. Primary impact damage has caused severe hemorrhagic contusion of the
left frontal lobe (C) - coup les...
Figure 23-13 Traumatic intracranial hemorrhages. A, Epidural hematoma (left) in which rupture of a meningeal artery, usual...
Epidural Hematoma
Epidural Hematoma
Middle Meningeal Artery
Bridging Veins
Subdural Hematoma
Subdural Hematoma
Acute Meningitis
Acute Bacterial Meningitis
Acute Meningitis
Infectious causes of chronic meningitis
• Tuberculosis
 Cryptococcosis
 Coccidioidomycosis
 Histoplasmosis
 Candidiasi...
Major causes of viral encephalitis in the United States
 Herpes simplex
 Mumps
 St. Louis

Geographical distribut...
Seasonal variation in infections capable of
causing viral encephalitis
HSV Encephalitis
Progressive Multifocal Leukoencephalopathy
Animal Cases of Rabies
Human Rabies Deaths
Tabes Dorsalis
Signs and symptoms of tabes dorsalis

Signs and symptoms
Pupillary abnormalities (Argyll R...
Prion diseases of humans and animals

Transmissible mink
encephalopathy (TME)
Chronic ...
 Propagation of scrapie PrP in neurons of the brain apparently occurs via

a domino effect on an internal membrane. A fav...
Characteristics of prion diseases and agents
 Prolonged incubation period of months to years
 Progressive course of week...
Spongiform Encephalopathy
Glioma of Brainstem (midbrain)
Glioma - Cerebrum
Glioblastoma Multiforme
Acoustic Nerve Schwannoma
Neurofibromatosis 1


>6 Cafe’-au-lait spots
Multiple Sclerosis
Cerebral Atrophy - Alzheimer’s Disease
AD - Hydrocephalus Ex Vacuo
AD - Neuritic Plaques
AD - Neurofibrillary Tangle
Huntington’s Disease
Huntington’s Disease
Huntington’s Disease
Parkinson’s Disease
Characteristics of Parkinsonism
 Rest tremor

Freezing of gait

Parkinson’s Disease
Parkinson’s Disease
Amyotrophic Lateral Sclerosis (ALS)
Upper & Lower Motor Neurons
ALS - Corticospinal Tract Degeneration
Wernicke's encephalopathy. In this coronal section of brain the mammillary bodies (arrows)
show petechial hemorrhages char...
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  • Note the large defect in the lower back region of this baby. This neural tube defect is so large that the spinal canal is open and the meninges and cord can extend out, making this a meningomyelocele. You may see the term "spina bifida" used to describe a more subtle defect seen on a radiograph in which there is incomplete closure but skin still covers the defect.
  • The surface of the brain with cerebral edema demonstrates widened gyri with a flattened surface. The sulci are narrowed. Treat with mannitol. If pupil or pupils begin to dilate then hyperventilate. Sometimes need to place ventricular catheter. No role for steroids unless this is vasogenic edema vs. cytotoxic edema.
  • Papilledema is shown here. Note that the margins of the optic disk are indistinct with blurring, because there is swelling with elevation of the optic nerve head. Any condition that increases intracranial pressure (edema, hemorrhage, mass lesions, etc) will produce papilledema.
  • Acute brain swelling in the closed cranial cavity is serious. Swelling of the left cerebral hemisphere has produced a shift with herniation of the uncus of the hippocampus (medial temporal lobe) through the tentorium, leading to the groove seen at the white arrow.
  • The end result of herniation is compression and Duret hemorrhages, as seen here in the pons.
  • Note the marked dilation of the cerebral ventricles. This is hydrocephalus. Hydrocephalus can be due to lack of absorption of CSF or due to an obstruction to flow of CSF. Hydrocephalus can be a long-term complication of infection. A basilar meningitis, for example, may lead to scarring that obstructs CSF outflow via the foramina of Luschka or Magendie. Inflammation with scarring of arachnoid granulations at the vertex may diminish CSF absorbtion.
  • Occurs at areas of turbulent blood flow (branching arteries)
  • This is an intermediate to remote infarct in the distribution of the middle cerebral artery.
  • Here is a cerebral infarct from an arterial embolus, which often leads to a hemorrhagic appearance. There is cytotoxic edema which obscures the structures. The acutely edematous infarcted tissue may produce a mass effect. Note the decrease in size of the lateral ventricle on the left, with shift of the midline to the right.
  • The infarction seen here has punctate hemorrhages. This infarct in the distribution of the middle cerebral artery was caused by an embolus from a left atrial mural thrombus in a patient with atrial fibrillation.
  • The bilaterally symmetric dark discolored areas seen superiorly and just lateral to the midline represent recent infarction in the watershed zone between anterior and middle cerebral arterial circulations. Such watershed infarctions can occur with relative or absolute hypoperfusion of the brain.
  • This intermediate infarct of the frontal lobe shows liquefactive necrosis with formation of cystic spaces as time passes and the process of resolution begins.
    LIQUEFACTIVE NECROSIS-results from the hydrolytic enzymes and occurs when autolysis and heterolysis prevail over conditions that favor denaturation of proteins which leads to cystic formation of the infarction
  • Hemorrhages involving the basal ganglia area (the putamen in particular) tend to be non-traumatic and caused by hypertension, which leads to arteriosclerosis that damages and weakens the small penetrating arteries. A mass effect from the collection of blood with midline shift, often with adjancent secondary edema, may lead to herniation.
  • Another cause for hemorrhage, particularly in persons aged 10 to 30, is a vascular malformation. Seen here is a mass of irregular, tortuous vessels over the left posterior parietal region.
  • Here is an incidental non-ruptured berry aneurysm located at the bifurcation of the left middle cerebral and anterior communicating arteries of the circle of Willis at the base of the brain. These aneurysms may be present in 1% of persons. They form at points where there is a developmental weakness in the arterial wall.
  • The circle of Willis has been dissected, and three berry aneurysms are seen. Multiple aneurysms are seen in about 20-30% of cases of berry aneurysm. Such aneurysms are "congenital" in the sense that the defect in the arterial wall is present from birth, but the actual aneurysm takes years to develop, so that rupture is most likely to occur in young to middle age adults.
  • The white arrow on the black card marks the site of a ruptured berry aneurysm in the circle of Willis. This is a major cause for subarachnoid hemorrhage at the base of the brain. As the weak wall of the artery, which lacks an internal elastic lamina and a media, expands to form the aneurysm, there may initially be leakage of blood that produces headaches, but there is risk for sudden rupture to produce a severe headache. The blood irritates the arteries to produce vasospasm and promote cerebral anoxia.
  • The subarachnoid hemorrhage from a ruptured aneurysm is more of an irritant producing vasospasm than a mass lesion.
  • Diffuse subarachnoid hemorrhage extends from the base of the brain to the lateral surface of frontal and temporal lobes. Note that there is no blood beneath the dura reflected upwards. A ruptured berry aneurysm with subarachnoid hemorrhage leads to sudden onset of an excruciating headache. The mortality rate with initial rupture is 25 to 50%
  • The orange-brown, scalloped appearance of these lesions is consistent with old contusions. The resolution left behind hemosiderin from the hemorrhage that produces the orange-brown staining.
  • The characteristic location of the hemorrhage in this brain is consistent with a fall forward resulting in a injury to the inferior frontal and temporal lobes. This has resulted in extensive contusions and subarachnoid hemorrhage.
  • A blood clot is seen over the external surface of the dura. Thus, this is an epidural hematoma. Such a location for hemorrhage is virtually always the result of trauma that causes a tear in the middle meningeal artery.
  • The skull has been removed to reveal the middle meningeal artery having emerged from the foramen spinosum and branching over the outer dura.
  • The dura has been reflected above to reveal the bridging veins that extend across to the superior aspect of the cerebral hemispheres. These can be torn with trauma, particularly if there is significant cerebral atrophy that exposes these veins even more.
  • The dura has been reflected back (with a small portion visible at the lower right) to reveal a subdural hematoma. Such a blood clot is usually the result of trauma with tearing of the bridging veins.
  • One cause for acute swelling is infection. The yellow-tan clouding of the meninges seen here is due to an exudate from acute meningitis.
  • The yellow-tan exudate of acute bacterial meningitis seen here obscures the sulci.
  • Here is another example of an acute meningitis from bacterial infection. The cerebrospinal fluid (CSF) obtained via lumbar puncture in such cases typically has a low glucose, high protein, and a cell count with many PMN's. A gram stain should be done to identify organisms
  • In temperate climates of the northern hemisphere, the viral encephalitides have distinct seasonal occurrences that may be helpful in the differential diagnosis. Encephalitis caused by the mosquito-borne and tick-borne arboviruses peaks in the spring and summer, paralleling the periods of activity for their insect vectors. Others, such as herpesvirus infections, may occur year round.
  • An uncommon but distinctive form of viral infection of the brain is herpes simplex virus encephalitis. The cases are sporadic and can occur in non-immunocompromised persons. HSV infection often produces hemorrhages in the temporal lobe.
  • There are areas of hemorrhage with brain swelling and a midline shift. This resulted from a disseminated Aspergillus fungal infection in a patient who was markedly neutropenic. The greenish discoloration has resulted from bile pigments (oxidized to biliverdin by formalin fixation) leaking past a blood-brain barrier destroyed by the invasive fungal hyphae.
  • Progressive multifocal leukoencephalopathy (PML) is an infection of the CNS caused by the JC papovavirus. PML occurs in immunocompromised patients, such as those with AIDS. PML appears grossly as irregular areas of granularity in white matter, which bear some resemblance to the plaques of demyelination with multiple sclerosis.
  • Raccoons, skunks, and bats
  • Early evidence of poliomyelitis from Middle Kingdom Egypt ca. 1300 BC. A tracing of one of the figures from the funerary stele of the priest Rom. The figure has a withered right leg and dropped foot, which are typical of poliomyelitis
  • Polio specifically effects anterior horn cells
  • LOCOMOTOR ATAXIA- posterior column infection : loss of position sense and pain sensation as seen in advanced neurosyphilis
  • ARGYLL ROBERTSON PUPIL-Light-Near dissociation (pupil constrict on convergence but not light
  • The prion diseases have also been referred to as transmissible spongiform encephalopathy agents. The first of these diseases, scrapie, was recognized to be transmissible in sheep in the 1930s. The latest epidemic of BSE in Britain, referred to by the lay public as "mad cow disease," is believed to have been transmitted to humans via the ingestion of contaminated beef resulting in a progressive dementia that has been named new variant CJD (nvCJD). The disease caused by nvCJD occurs in younger people and disease progression is slower. Kuru is of historical interest because it was the first human prion disease to be recognized as transmissible. It occurs in the Fore Indians of New Guinea beginning with gait, trunk, and limb ataxia and involuntary movements (myoclonus, chorea, tremor) followed by dementia at a later date. Because it is transmitted primarily through cannibalistic rituals, which are now restricted, kuru is rare.
  • One of the important characteristics of these agents is that they do not contain detectable nucleic acids (DNA, RNA) but do contain a protein, the prion protein (PrP), that must be transmitted for disease to occur. This finding led to the "prion" terminology, which was derived from "protein" and "infectious." There is no specific treatment for the various prion diseases. However, the agent (prions) can be disinfected with various sterilization procedures.
  • The "holes" in the cortex of the cerebrum seen here represent a spongiform encephalopathy known as Jacob-Creutzfeldt disease (CJD). This is a form of rapidly progressive dementia. It is due to a poorly understood prion protein that has infectious potential, but the cases appear sporadically (1 in a million). SWISS CHEESE APPEARANCE
  • Seen here is a metastasis from a lung carcinoma. Metastases most often appear at the border of the grey and white matter in the distribution of the middle cerebral artery, as in this case, because that is where the blood flow (vascular distribution) is most likely to take metastases.
  • This sagittal section of brain demonstrates a large brainstem glioma. Most gliomas are astrocytomas.
  • This glioma is arising in the cerebral hemisphere. As in most gliomas, it is difficult to tell where the margin is.
  • This is the worst possible form of glioma--a glioblastoma multiforme (GBM). These neoplasms are quite vascular with prominent areas of necrosis and hemorrhage. Note how this one has crossed the midline to the opposite hemisphere.
  • Note how this meningioma beneath the dura has compressed the underlying cerebral hemisphere. Rarely, meningiomas can be more aggressive and invade.
  • This discrete firm neoplasm was removed from the surface of a peripheral nerve. It is a schwannoma (neurilemmoma) which arises from the nerve sheath Schwann cells
  • The mass lesion here is arising in the acoustic (eighth cranial) nerve at the cerebellopontine angle. This is a schwannoma. Patients may present with hearing loss. These benign neoplasms can be removed.
    May be referred to as acoustic neuroma
  • Note café-au-lait spots
  • Here is a demyelinated plaque in a patient with multiple sclerosis (MS). The lesions can be seen with MRI scans, but the appearance in the CSF of increased protein from increased IgG that demonstrates oligoclonal bands on electrophoresis is very consistent with this diagnosis.
  • The cerebral atrophy seen here mainly in the frontal and parietal regions is characterized by narrowed gyri and widened sulci. The atrophy seen here was due to senile dementia of the Alzheimer type (Alzheimer disease).
  • The cortical atrophy leads to compensatory dilation of the cerebral ventricles known as "hydrocephalus ex vacuo".
  • The characteristic microscopic findings of Alzheimer disease include neuritic plaques ("senile plaques") which are extracellular deposits of the amyloid beta-protein (Aァ). In the more numerous, smaller diffuse plaques this Aァ alone is present as filamentous masses. However, the diagnostic neuritic plaques also have dystrophic dilated and tortuous neurites, microglia, and surrounding reactive astrocytes.
  • This is a neurofibrillary "tangle" of Alzheimer disease. The tangle appears as long pink filaments in the cytoplasm. Neurofibrillary tangles are composed of cytoskeletal intermediate filaments in the form of hyperphosphorylated microtubule-associated proteins known as tau.
  • Scientists have discovered that the abnormal protein produced by the Huntington's disease gene, which contains an elongated stretch of amino acids called glutamines, binds more tightly to HAP-1 than the normal protein does. This molecular partnership may contribute to the debilitating symptoms associated with the disease./When the HD gene was found, researchers discovered that HD belongs to a newly discovered family of diseases called "triplet repeat" diseases. A gene's DNA bears coding molecules which are translated into specific amino acids, the building blocks of proteins. In the HD gene, the coding molecules cytosine, adenine, and guanine (CAG) - the triplet - repeat in a stretch more than they do in the normal gene. Normally the CAG sequence repeats between 11 and 30 times. People with HD may have CAG repeated between 36 and 125 times. The onset of the disease generally is in the 30s and 40s (with a range of age 2 to 82), but more than 60 repeats of CAG often are associated with an onset of HD before age 20. With the majority of people who have fewer than 60 repeats, there is great variability. A person can have 40 CAG repeats in his or her DNA sequence and have onset at age 17 or 70. On average, however, a feature dubbed "genetic anticipation" occurs. Each time the unstable DNA is passed on to offspring, the affected person experiences an earlier onset. ハハハハハ Scientists discovered that the HD gene produces a protein called huntingtin. This protein occurs in cells and is found throughout the body -- not just in the brain where there is heavy damage. The abnormal form of huntingtin is likely to have a mutated structure, perhaps causing an altered "polar zipper." This term is used to describe how the structure's string of polar or waterloving amino acids folds together like a zipper (see illustration) which may change its interactions with other proteins.
  • Atrophy of the head of the caudate nucleus leads to ventricular enlargement.
  • During movement, signals pass from the brain's cortex, via reticular formation and spinal cord (pathway A), to muscles, which contract. Other signals pass, by pathway B, to the basal ganglia; these damp the signals in pathway A, reducing muscle tone so that movement is not jerky. Dopamine, a nerve transmitter made in the basal ganglia, is needed for this damping effect. Another transmitter, acetylcholine, inhibits the damping effect.Parkinson's disease. In Parkinson's disease, degeneration of parts of the basal ganglia causes a lack of dopamine within this part of the brain. The basal ganglia are thus prevented from modifying the nerve pathways that control muscle contraction. As a result, the muscles are overly tense, causing tremor, joint rigidity, and slow movement. Most drug treatments increase the level of dopamine in the brain or oppose the action of acetylcholine.
  • The loss of pigmentation in the substantia nigra of the midbrain at the left in a patient with Parkinson disease is contrasted with a normal midbrain at the right.
  • At the left, normal numbers of neurons in the subtantia nigra are normally pigmented. At the right, there is loss of neurons and loss of melanin pigmentation with Parkinson disease.
  • A variety of cellular insults may intersect, leading individually or in concert to neuron degeneration, neuron death and finally ALS. A faculty gene (1) and excess glutamate (2) may lead to damaging free radicals (3), which can harm the nerve cell's DNA. Glutamate also may lead to the production of detrimental calcium, which can churn out its own supply of DNA-harming free radicals. The free radicals also may injure neurofilaments (4), proteins that serve as the skeleton of the cell. In addition, the immune system (5) may be involved in harming neurons. Abnormalities can lead to an accumulation of the toxic calcium.
  • Grossly, the corticospinal tracts in these cross sections of thoracic spinal cord demonstrate a pale white appearance from the degeneration resulting from amyotrophic lateral sclerosis (ALS).
  • Amyotrophic lateral sclerosis (ALS) is uncommon. It usually begins in middle age and proceeds to death in several years. There is loss of anterior horn cells, so that patients present with progressive weakness that proceeds to paralysis from neurogenic muscular atrophy. Because of the loss of anterior horn cells, the anterior (ventral) spinal motor nerve roots with ALS demonstrate atrophy, as seen here in comparison with a normal spinal cord motor nerve roots.

    1. 1. MEDEX 452: Pathophysiology for Primary Care Henry Stoll, PA-C
    2. 2. Anencephaly
    3. 3. Anencephaly
    4. 4. Spinal Cord Defects
    5. 5. Meningomyelocele
    6. 6. Cerebral Edema
    7. 7. Papilledema
    8. 8. Results of Increased Intracranial Pressure (ICP)
    9. 9. Uncal Herniation
    10. 10. Herniation
    11. 11. Hydrocephalus -- Causes
    12. 12. Hydrocephalus
    13. 13. Hydrocephalus - Ventricular Enlargement
    14. 14. Hydrocephalus - Results
    15. 15. Brain Blood Supply
    16. 16. Common Sites of Atherosclerosis
    17. 17. Common Sources of Emboli
    18. 18. Stroke - Middle Cerebral Artery
    19. 19. Thrombosis - Internal Carotid Artery
    20. 20. Embolic Stroke with Edema
    21. 21. Embolic Stroke with Punctate Hemorrhages
    22. 22. Watershed Infarctions
    23. 23. Liquefactive Necrosis with Cysts
    24. 24. Basal Ganglia Hemorrhage Due to Hypertension
    25. 25. AV Malformation
    26. 26. Berry Aneurysm Carotid bifurcation aneurysm
    27. 27. Figure 23-9 Relative frequency of common sites of saccular (berry) aneurysms in the circle of Willis. Downloaded from: StudentConsult (on 22 August 2008 07:07 PM) © 2005 Elsevier
    28. 28. Giant Aneurysms
    29. 29. Ruptured PCOM Aneurysm
    30. 30. Subarachnoid Hemorrhage
    31. 31. Subarachnoid Hemorrhage
    32. 32. Contusions
    33. 33. Cerebral contusions. Primary impact damage has caused severe hemorrhagic contusion of the left frontal lobe (C) - coup lesion, with smaller contusions on the right parietal lobe (P) contrecoup lesion. Swelling of the left side of the brain has caused cerebral herniation with compression of the midbrain
    34. 34. Figure 23-13 Traumatic intracranial hemorrhages. A, Epidural hematoma (left) in which rupture of a meningeal artery, usually associated with a skull fracture, leads to accumulation of arterial blood between the dura and the skull. In a subdural hematoma (right), damage to bridging veins between the brain and the superior sagittal sinus leads to the accumulation of blood between the dura and the arachnoid. B, Epidural hematoma covering a portion of the dura. C, Large organizing subdural hematoma attached to the dura. (B, Courtesy of Dr. Raymond D. Adams, Massachusetts General Hospital, Boston, Massachusetts.) Downloaded from: StudentConsult (on 22 August 2008 07:07 PM) © 2005 Elsevier
    35. 35. Epidural Hematoma
    36. 36. Epidural Hematoma
    37. 37. Middle Meningeal Artery
    38. 38. Bridging Veins
    39. 39. Subdural Hematoma
    40. 40. Subdural Hematoma
    41. 41. Acute Meningitis
    42. 42. Acute Bacterial Meningitis
    43. 43. Acute Meningitis
    44. 44. Infectious causes of chronic meningitis • Tuberculosis  Cryptococcosis  Coccidioidomycosis  Histoplasmosis  Candidiasis  Blastomycosis  Syphilis  Brucellosis  Toxoplasmosis  Nocardiosis  Lyme disease  Actinomycosis
    45. 45. Major causes of viral encephalitis in the United States Virus  Herpes simplex  Mumps  St. Louis Geographical distribution Nationwide Nationwide Nationwide (esp. south and central)  California/La Crosse Central and eastern US  Western equine Western US  Eastern equine Atlantic and Gulf coasts  Colorado tick fever Western US  Venezuelan equine Texas and Florida  Rabies Nationwide
    46. 46. Seasonal variation in infections capable of causing viral encephalitis
    47. 47. HSV Encephalitis
    48. 48. Aspergillus
    49. 49. Progressive Multifocal Leukoencephalopathy
    50. 50. Rabies
    51. 51. Animal Cases of Rabies
    52. 52. Human Rabies Deaths
    53. 53. Poliomyelitis
    54. 54. Poliomyelitis
    55. 55. Poliomyelitis
    56. 56. Poliomyelitis
    57. 57. Poliomyelitis
    58. 58. Tabes Dorsalis
    59. 59. Signs and symptoms of tabes dorsalis                 Signs and symptoms Pupillary abnormalities (Argyll Robertson pupils) Absent reflexes, lower extremities Lightning pains Romberg's sign Impaired position sense Ataxia Bladder disturbances Visual loss Impaired vibratory sense Visceral crisis Impaired pain sense Cranial nerve palsy Paresthesias Charcot joints Anal sphincter atony Perforating ulcers (mal perforans) Range, % 94-97 78-94 70-75 51-55 44-45 42-46 28-33 16-43 17-52 15-18 13-18 9-10 7-24 6-7 3-14 5-6
    60. 60. Prion diseases of humans and animals           Disease Scrapie Transmissible mink encephalopathy (TME) Chronic wasting disease Bovine spongiform encephalopathy (BSE) Feline spongiform encephalopathy (FSE) Kuru Creutzfeldt-Jakob disease (CJD) New variant CJD (nvCJD) Gerstmann-Straussler syndrome (GSS) Fatal familial insomnia (FFI) Host Sheep, goats Mink Mule deer, elk Cattle Cats Humans Humans Humans Humans Humans
    61. 61.  Propagation of scrapie PrP in neurons of the brain apparently occurs via a domino effect on an internal membrane. A favored hypothesis holds that the process begins (a) when one molecule of scrapie (red) contacts a normal PrP molecule (brown) and (b) induces it to refold into the scrapie conformation. Then, the scrapie particles attack other normal PrP molecules (c). Those molecules, in turn, attack other normal molecules and so on (broken arrow) until scrapie PrP accumulation reaches dangerous levels (d).
    62. 62. Characteristics of prion diseases and agents  Prolonged incubation period of months to years  Progressive course of weeks to months to death  No host immune response (except astrocytosis)  Pathologic lesions confined to the central nervous system  Similar histopathology  No specific treatment Causative agents (prions) have specific properties:  No detectable nucleic acid  Resistant to alcohol, formalin, heat, ultraviolet (UV) irradiation, nucleases*  Susceptible to proteolytic enzymes, denaturing agents, organic solvents** Sterilized by:  Steam autoclaving 1 hour at 132ºC  Immersion in 1N NaOH for 1 hour at room temperature *Agents that hydrolyze or modify nucleic acids. **Agents that digest, denature, or modify proteins
    63. 63. Spongiform Encephalopathy
    64. 64. Metastasis
    65. 65. Glioma of Brainstem (midbrain)
    66. 66. Glioma - Cerebrum
    67. 67. Glioblastoma Multiforme
    68. 68. Meningioma
    69. 69. Schwannoma
    70. 70. Acoustic Nerve Schwannoma
    71. 71. Neurofibromatosis 1
    72. 72. NEUROFIBROMATOSIS DIAGNOSTIC CRITERIA TWO OR MORE OF THE FOLLOWING NF-1(VONRECKLINGHAUSENS’NFT) >6 Cafe’-au-lait spots >2 neurofibromas Inguinal/axillary freckles Optic glioma >2 Lisch nodules Sphenoid dysplasia 1st degree relative NF-2 Bilateral eigth nerve masses or two of the follwing  Neurofibroma  Meningioma  Glioma  Schwannoma  Juvenile cateract
    73. 73. Neurofibromatosis
    74. 74. Neurofibromatosis
    75. 75. Multiple Sclerosis
    76. 76. Cerebral Atrophy - Alzheimer’s Disease
    77. 77. AD - Hydrocephalus Ex Vacuo
    78. 78. AD - Neuritic Plaques
    79. 79. AD - Neurofibrillary Tangle
    80. 80. Huntington’s Disease
    81. 81. Huntington’s Disease
    82. 82. Huntington’s Disease
    83. 83. Parkinson’s Disease
    84. 84. Characteristics of Parkinsonism Major Features  Rest tremor Motor Freezing of gait Autonomic Cognitive Urinary Slowness in thinking  Rigidity Dystonia Constipation Dementia  Bradykinesia Muscle ache Impotence in men Depression  Loss of postural Kyphosis reflexes
    85. 85. Parkinson’s Disease
    86. 86. Parkinson’s Disease
    87. 87. Amyotrophic Lateral Sclerosis (ALS)
    88. 88. Upper & Lower Motor Neurons
    89. 89. ALS - Corticospinal Tract Degeneration
    90. 90. Wernicke's encephalopathy. In this coronal section of brain the mammillary bodies (arrows) show petechial hemorrhages characteristic of acute Wernicke's encephalopathy caused by thiamine deficiency