CNS I Path - Random stuff and LAB MED Flashcards
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
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
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
Infectious Diseases
Meningitis, Encephalitis, Abscess
Overlap almost entirely with vascular
EXCEPT ABSCESS can also present as SLOWLY PROGRESSING COGNITIVE LOSS
Not very acute
Traumatic Diseases
Epidural and Subdural Hematomas
Epidural = ACUTE
Subdural = Can progress insidiously!!! So slow cognitive loss is possible
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
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)
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
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
Acute or Subacute Neuro Symptoms (headache, seizure, cognitive loss, aphasia, sensory loss, visual loss, tremor)….
VASCULAR or INFECTIOUS or TRAUMATIC or NEOPLASTIC
Progressive cognitive loss RULES OUT…
Abscess
Subdural hemorrhage (trauma)
Degenerative (all of them!!!)
Neoplasms (except maybe Metastases)
Proximal Weakness is suggestive of…
MYOSITIS
Peripheral Neuropathy in a stocking glove distribution…
GBS (acute), CIDP (chronic), DIABETIC NEUROPATHY
If unknown which one (CIDP or DM) –> NERVE biopsy
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)
What are Charcot-Bouchard aneurysms?
HTN damage, ruptures into the PARENCHYMA
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!
