CNS I Path - Random stuff and LAB MED Flashcards by Connor Benton

What are the 8 Categories of CNS disease?

VITAMINS

V = Vascular
I = Infectious
T = Trauma
A = Autoimmune
M = Metabolic/Toxic
I = Idiopathic/Genetic
N = Neoplastic

D = Neurodegenerative

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Cardinal Symptoms of CNS diseases (tell us where diseases are)

Headache, Seizures, Cognitive Loss = Cortical symptoms

Aphasia, Weakness = Frontal Lobes

Sensory loss = Parietal Lobe

Visual Loss = Occipital Lobe

Tremors = Cerebellum

Proximal Weakness = Muscle Disease

Stocking Glove Syndrome = Distal Peripheral Nerve

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Vascular Diseases

Tend to present ACUTELY

Headache, seizure, aphasia, hemiparesis, hemisensory loss, visual loss, tremor

For stroke –> give tPA –> rule out others as they are ALL BLEEDS and could get worse with tPA!

We learned about ischemic infarctions, hemorrhage, ruptured AV malformations, aneurysms

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Infectious Diseases

Meningitis, Encephalitis, Abscess

Overlap almost entirely with vascular

EXCEPT ABSCESS can also present as SLOWLY PROGRESSING COGNITIVE LOSS

Not very acute

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Traumatic Diseases

Epidural and Subdural Hematomas

Epidural = ACUTE

Subdural = Can progress insidiously!!! So slow cognitive loss is possible

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Autoimmune Diseases

MS (central demyelination), GBS (Acute PNS demyelination), CIDP (chronic PNS), Polymyositis (inflammation of the muscle

Presentation is variable

MS = only one acting on the CNS

CIDP and GBS = Differ based on their onset (chronic and acute respectively) of peripheral neuropathy

Polymyositis = Difficult raising arms or using the stairs

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Metabolic Diseases

Diabetes –> one of the most common causes of peripheral neuropathy

Hyper/hypoglycemia can have a wide range of CNS effects (headaches, dizziness, seizures)

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Idiopathic/Congenital

AD, PD, Lewy Body Dementia, Frontal Temporal Dementia, ALS

ALL PRESENT WITH SLOOOOW COGNITIVE LOSS

ALS has the mildest loss - mainly attacks motor neurons until very late, so if they present with sensory symptoms DONT THINK ALS first

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Neoplasms of CNS

Gliomas and Ependymomas (primary); Meningiomas; Metastases

Present ALL VERY SIMILARLY, potentially hitting every single cardinal symptom!

METS are usually FAST, so cognitive decline may be faster than others

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Acute or Subacute Neuro Symptoms (headache, seizure, cognitive loss, aphasia, sensory loss, visual loss, tremor)….

VASCULAR or INFECTIOUS or TRAUMATIC or NEOPLASTIC

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Progressive cognitive loss RULES OUT…

Abscess

Subdural hemorrhage (trauma)

Degenerative (all of them!!!)

Neoplasms (except maybe Metastases)

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Proximal Weakness is suggestive of…

MYOSITIS

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Peripheral Neuropathy in a stocking glove distribution…

GBS (acute), CIDP (chronic), DIABETIC NEUROPATHY

If unknown which one (CIDP or DM) –> NERVE biopsy

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Lumbar Punctures?

NEVER DO ONE BEFORE A CT –> need to RULE OUT a mass or an abscess

LP with a mass or an abscess could build up lots of pressure and CAUSE HERNIATION!

Also, CT can’t differentiate abscesses from masses (biopsy)

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What are Charcot-Bouchard aneurysms?

HTN damage, ruptures into the PARENCHYMA

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Bridging Veins and Berry Aneurysms?

Bridging rupture will result in SUBDURAL bleeds

Berry aneurysms –> SUBARACHNOID bleeds

Meningitis Diagnosis

Cannot exist WITHOUT SPINAL TAP

Stains

Nissl Stain –> Large motor neurons –> highlights Nissl bodies (RER)

Cajal Silver Stain –> highlight neurons, first type of stain

Luxol Fast blue –> used to identify demyelinating lesions

H&E –> used for normal tissue and most common

Hypoxia/Ischemia of Neuronal Tissue

Strokes cause this, for example

Neuronal chromatin CONDENSES, resulting in a dark nucleus

Neuronal cytoplasm becomes HIGHLY EOSINOPHILIC

Neuronal cell bodies SHRINK and RETRACT from the neuropil, resulting in a clear space around the cell body

RED DEAD NEURONS result –

Time course after cerebral infarct

Neurophils invade acutely for up to 3 days following insult

Between days 3-5, macrophages enter to begin the SUBACUTE response, clearing damaged tissue

Soon after, REACTIVE ASTROCYTES begin to WALL OFF THE INFARCT, forming a GLIAL SCAR –> Liquefactive necrosis results in a fluid filled cyst, which is walled off by the scar

In the PNS, nerves have the capacity to

REGENERATE

Common INCLUSIONS

AD –> NFTs (Tau) and Beta Amyloid

PD –> LEWY BODIES!!!!

Herpes Infection –> COWDRY TYPE A INCLUSION BODIES

Rabies –> NEGRI BODIES

ALS –> BUNINA BODIES

Types of Cerebral Edema

VASOGENIC and CYTOTOXIC

Vasogenic Edema

Site of injury = Cerebral blood vessels

localization = mostly white matter

Vascular permeability = Increased, leading to leakage of plasma proteins

Features = Enlarged extracellular spaces, swollen astrocytes

Fluid = Plasma filtrate, including serum proteins

Causes = Vessel trauma, tumors, ischemia/hypoxia, infection

Cytotoxic Edema

Site = brain parenchyma Localization = Gray or White matter depending on cytotoxic agent Vascular permeability? not changed Features --> extracellular space UNCHANGED; swollen cells depend on the agent Fluid = plasma ultrafiltrate, composition depends on cytotoxic agent Causes = Various cytotoxic agents

WBCs/RBCs in CSF

Eosinophils -- Parasitic Neutrophils -- Bacterial Lymphocutes -- Viral RBCs -- PROBABLY ERROR, if not --> Subarachnoid hemorrhage!

CSF Glucose

CSF GLUCOSE SHOULD BE 2/3 that of SERUM GLUCOSE --> Higher in diabetics, so make sure you know that Low CSF glucose = bacterial meningitis, TB, fungal infection

EEG

Electroencephalography allows us to evaluate the brain's electrical activity and is used in the evaluation of seizures. Evoked potentials serve as a way to evaluate the electrical integrity of the visual, sensory and auditory systems. NOT USEFUL FOR HEADACHES Polysomnograms --> allow for evaluation of sleep apnea and headaches

What would bilateral papilledema indicate in a patient with headaches?

Increased ICP!!!! Papilledema takes a week or so to develop -- not a sudden acute problem; The optic nerve is normally surrounded by subarachnoid fluid. As intracranial pressure rises, the area around the nerve will swell. Remember, the cell bodies for CN II are in the retina! The retinal ganglia cells get backed up due to the increased pressure on the nerve, and the result is built up axoplasmic flow. GET MRI or CT!!!! patient could go blind! DONT DO SPINAL TAP FIRST

What is a cause of MORNING HEADACHES?

SLEEP APNEA!!!! Get a POLYSOMNOGRAM! Morning headaches are indicative of increased cerebrospinal fluid and cerebral swelling in lying down/recumbent positions. Neoplasms can also cause this as well!

* A 65 year old man presents with bitemporal headaches of 6 months duration * Occasionally associated with very mild elevations in temperature * Some achiness of shoulders and proximal arms for 3 months * Exam notable for temporal tenderness

GIANT CELL ARTERITIS! -- Specifically temporal arteritis Achiness = Polymyalgia Rheumatic (commonly associated with temporal arteritis) SEDIMENTATION RATE is HIGH in this condition (rate at which RBCs fall in test tube --> 0 = floating, HIGH = fall very fast) RBCs sediment fast because ACUTE PHASE PROTEINS attach and make them fall quicker

Meningitis Values

The difference between the fungal and viral infections is the glucose (lower in fungal/TB, normal in Viral)!! Bacterial infections usually have over 1000 WBC, and will be mostly neutrophils (also have LOW glucose) Viral infections will have a lower WBC, though still elevated, but will be mostly lymphocytes Protein elevated in ALL OF THEM (Fungal/TB especially)

When MUST you do an LP?!

WHEN PATIENT COMES IN WITH WORST HEADACHE OF THEIR LIFE (SUBARACHNOID) CT will MISS 5-10% of all SAH!