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Slide 1

  • Spinal cord cross section
  • Butterfly pattern = grey matter, the area surrounding it is white matter (containing tracts/columns)
  • Surrounding them are meninges made of collagen (dura mater+subdural space, arachnoid mater+subarachoind space then pia mater) that wraps the whole CNS
    • In the subarachnoid space live blood vessels, and nerve rootlets
  • Dorsal horn is smaller wing, and anteriorly is the ventral horn which is motor (larger wing)
    • Note that motor includes both muscles and glands
  • Central canal contains CSF
  • Ependymal cells surrounding central canal secretes CSF (so does the choroid plexus which is the inferior medullary velum)
  • Ventral horn
    • Motor neurons
    • Cell bodies (somata) with extensions (axons)
    • Note that dark dot = nucleolus, not nucleus
    • Dots that look like pepper = Nissl granules (rER)
    • Axon hillock = region with no Nissl granules. This tells us that the process coming away from the soma is an axon (if there are Nissl granules in the process, then it's a dendrite)
    • Somata that appear anucleate are cut above or below the level of the nucleolus/nucleus
    • Supporting cells (glial cells) = nuclei of oligodendrocytes (supporting cell that myelinates - similar to Schwann cell in PNS). Small cells. Larger nucleus = nucleus of an astrocyte (part of blood brain barrier, and involved in repair after injury)
  • Taking a line across from the ventral horn are the dorsal rootlets. Similarly, taking a line from the ventral horn we can see the ventral rootlets
    • We'll see a ganglion later on (the trigeminal ganglion)
  • Note that astrocytes/glia are present in both ventral and dorsal horns

  • Cell body (soma, perikaryon) is the region of the neuron containing a large pale-staining spherical, nucleus with a conspicuous nucleolus and perinuclear cytoplasm.
  • Dendrites project from the cell body and are specialized for receiving (afferent) stimuli from sensory cells, axons and other neurons which are then transmitted towards the soma.
  • Axons arise as a single thin process extending longer distances from the cell body than the dendrite. As with dendrites, the terminals of the axon are branching and terminate in end bulbs (terminal boutons), which come close to another cell and form a synapse.
  • Peripheral Nerve Fibers
    • Peripheral nerves are bundles (fascicles) of nerve fibers (axons) surrounded by several CT sheaths. Each bundle contains sensory and motor components.
    • Myelinated Fibers (1-20μm diameter)
    • Myelin (rich in lipid) is the membrane of the Schwann cell organized into a spiral sheath that is wrapped several times around the axon. Schwann cells are cells whose cytoplasm contains a flattened nucleus, a small Golgi apparatus, and a few mitochondria. Myelinated fibers are capable of rapid transfer of impulses (touch sensory pathways).
    • Unmyelinated Fibers (less than 2μm in diameter)
    • Some axons in the PNS are surrounded by Schwann cells but not wrapped with layers of myelin. They are found in pain and temperature sensory pathways and motor paths to the viscera.
  • Neuropil is an area of the nervous system consisting mostly of unmyelinated axons, dendrites and glial cells. Basically it's the meshwork of all the neural structures except for the cell bodies. I.e. grey matter = cell bodies + neuropil.


Slide 2

  • Spinal cord smear
  • Can see somata, axons and Nissl granules (which aren't present in axon hillocks)
  • Lots of dendrites - important for neuroplasticity

Slide 3

Note in old notes

  • Trigeminal ganglion
  • Pseudounipolar somata, central nucleus
  • Satellite cells surrounding somata
  • Can see axon hillock, devoid of Nissl granules
  • Some cells are undergoing apoptosis (appear ragged)
  • Lipofuscin appears as brown stain in the cells (indicator of age)
  • Note axon with myelin around it. Appears as a fishbone.
    • Schmidt Lanterman cleft is a space that is a remnant of the myelin sheath, where the Schwann cell tapers as it wraps around the axon. This allows the nerve to stretch
      • Regions within compact myelin in which the cytoplasmic faces of the enveloping myelin sheath are not tightly juxtaposed, and include cytoplasm from the cell responsible for making the myelin. Schmidt-Lanterman incisures occur in the compact myelin internode, while lateral loops are analogous structures found in the paranodal region adjacent to the nodes of Ranvier.
  • Neurokeratin is the protein structure that is present in the myelin sheath

Slide 4

  • Cerebellum
  • Folds (folium) like a leaf
  • Can see the meninges (damaged) - mainly can see arachnoid and pia mater (dura stripped off)
  • Blood vessels present
  • White matter = tree branches on the inside. Grey matter is on the outside of that, subdivided into layers
  • Grey matter layers
  1. Inner granular layer - most # of cells in CNS, takes mossy fibres from deep pontine nuclei to dendritic tree of Purkinje cells
  2. Middle Purkinje cells with an extensive dendritic network, but very small axons
  3. Outer molecular layer - axon terminals (other parts of brain e.g. cerebrospinal tract, dendrites of Purkinje cells, glial cells)
  • Fourth ventricle and choroid plexus (producing CSF)
  • Brainstem


Slide 5

  • Cerebellum again

Slide 6

  • Peripheral nerve in cross section and longitudinal section
  • Peripheral nerves live in bundles (fascicles)
    • Adipose tissue/adipocytes often travel with nerves, as do blood vessels
    • Neurovascular bundle
  • 3 fascicles with nerves inside them
  • 3 levels of CT surrounding the bundles of axons that make up the nerve:
    • Endoneurium - wraps each axon directly
    • Perineurium - wraps the whole axon bundle
    • Epineurium - wraps all the perineurium-wrapped bundles
  • These compartmentalise the nerves and restrict infections: similar layers around muscle (endomysium etc); collagen wrappings are made of fibroblasts
  • Schwann cell nuclei are shaped like a banana, and make myelin. Myelin is absent as it dissolves in preparation - you see the axon surrounded by a space
    • Schwann cell in periphery is equivalent to oligodendrocyte in CNS
  • Majority of these cells are myelinated
  • A nerve is twisted (not a straight cable), enabling it to stretch. Some of the fibres therefore appear out of focus
  • Blood vessels - surrounded by smooth muscle

A nerve cut in longitudinal and cross section

Types of neural CT wrapping
  • 3 bundles (fascicles)
  • outside – stringly pink collagen wrapping
  • Nerves and muscles have 3 levels of wrapping
    • Endoneurium = tiny collagen around the axon
    • Perineurium = surrounds bunch of axons (fascicle)
    • Epineurium = Surround entire nerve (several fascicles)
    • Some nerves with only one bundle have only a perineurium and no epineurium
  • Wrapping helps stop infection from spreading
  • Wrapping at the top of the slide – perineurium?
  • Axons - disappears quickly – but may come back
  • Fishbone like structure – schwann cells – myelin disappears but the neurokeratin remain (spines).
    • In between them are Schmidt Lanterman clefts where myelin used to be.
      • Associated with coiled wrapping of the myelin that Schwann cells do.

Nerve in cross section – neurovascular bundle

  • 3 fascicles of nerves, blood vessel with fat (adipose cells)
  • collagen – perineurium
  • epineurium on outer edge of slide
  • inside a fascicle – can see blood vessels, and axons with surrounding space where myelin used to be
  • (think of cables)
  • Dark cells crescent shaped – schwann cell nucleus which make the myelin.
  • Nuclei:
    • Schwann cells
    • Fibroblasts: generates connective tissue components in which axons are embedded
    • Endothelial cells (for blood vessels)
    • Smooth muscle cells.



Case 1

A 56-year-old man was admitted to hospital through the Casualty department after an hour-long episode of dull, central chest pain at rest accompanied by shortness of breath and profuse sweating. → SIGNS OF M.I .He was investigated and treated for myocardial infarction, and appeared to be slowly recovering until 6 days later, when he developed right-sided hemiparesis and severe aphasia. His level of consciousness deteriorated, and he died 3 weeks later.

  • How did this happen?
    • MI (6 days ago)
    • → mural thrombus over site of infarction → breaks off → embolism
    • Atrial fibrillation (also predisposes to thrombus and embolism)
    • → reduced cardiac output leading to systemic hypotension and failure of perfusion of brain
  • Other concerns:
    • MI is due to atherosclerosis: which also a high risk factor for CVA
  • Symptoms:
    • Hemiparesis (weakness on one side of body)
    • Aphasia (cannot speak)
      • → L hemisphere, Broca’s area
      • implies an infarction of the left MCA; due to a mural thrombus in LV after MI. Mural thrombus could have embolised from heart -> MCA is the most direct path from the internal carotid artery.
        • large embolus that impacted quite proximally as it has affected a large area of the MCA
  • Cause of death:
    • Unlikely to be cerebral oedema and ICP → herniations (cerebellar tonsils - tonsillar herniation; compresses the medulla oblongata+respiratory/cardiac centres within it); as oedema is maximal after 4-6 days [3 weeks after]
    • Most likely due to complications of stroke such as bed ridden → DVT [pulmonary embolism] or pneumonia
    • Sepsis - due to catheterisation (immobility) or bronchopneumonia (aspiration of food or water, immobility)



Three regions

  1. Zone of liquefactive necrosis (top). Don't know why liquefactive necrosis occurs rather than coagulative necrosis.
    • No nuclei or architecture
    • No neutrophils or pus (this is the one situation where you have liquefaction in the absence of neutrophils)
    • Fat macrophage cells which have phagocytosed myelin - may be local or have migrated. Phagocytose debris from necrotic material. Gittezellen
  2. Zone of gliosis (healing)
    • Increased cellularity (gliosis)
    • No neuronal cell bodies
    • Fluid accumulation
    • Neuropil damage
    • Astrocyte actively making proteins/repair. These have plump eosinophilic cytoplasm. These cells are producing lots of proteins and fibrillary cytoplasmic proteins to wall off the area of infarction. Gliosis is better than scarring because scarring produces scar contraction (distorts axonal tracts - further impairment of function). Reactive astrocytes tend to have large nuclei that are pale-staining with prominent nucleoli. AKA germistacytic astrocytes.
  3. Zone of normal cortex
    • Pink - neuropil region with axons, dendrites, glial cells and stroma; full of protein - eosinophilic
    • Around the blood vessels, there is usually a potential space (Vierkow Robans space) - it is enlarged here, indicating oedema (potential cause of complications following cerebral infarction.

Adaptive tutorial

  • 1. The region of attempted healing is highlighted in red. This region is recognisable by increased numbers of cells with eosinophilic cytoplasm, as well as increased vascularity and oedema.
  • 2. The region of normal cerebral cortex is highlighted in blue. This region is recognisable by the presence of intact neuronal cell bodies.
  • 3. The region of necrosis is highlighted in green. This region is recognisable at low magnification by the loss of tissue structure.
  • Liquefactive necrosis most commonly occurs as a consequence of pyogenic bacterial infection, leading to the formation of pus.
  • In this case, liquefactive necrosis in the cerebrum has occurred as a consequence of ischaemic injury. In all other tissues, prolonged ischaemic injury leads to coagulative necrosis.
  • The reasons for the different response in the cerebrum are unclear, but might be related to high concentrations of lysosomal enzymes within neurons, resulting in liquefaction after neuronal cell death.
  • Macrophages containing lipid: In this field there are many plump macrophages/microglial cells with foamy cytoplasm as a result of phagocytosis of phospholipids and myelin. This material was derived from the cell membranes of necrotic neurons and oligodendrocytes.
  • Reactive astrocytes: The cells with eosinophilic cytoplasm are indeed reactive (gemistocytic) astrocytes. These cells produce fibrillar processes that wall off areas of necrosis within the CNS.
    • This is known as healing by gliosis, as opposed to healing by fibrosis in other tissues.
    • The advantage of gliosis in the CNS is that there is no contraction by glial cells (unlike fibroblasts), which might distort surviving axonal tracts.
  • Red neurons - Red neurons are neurons that are undergoing cell death. Acute shrinkage, angularity, and homogeneous eosinophilia of the cytoplasm. The nucleus becomes shriveled, pyknotic and hyperchromatic. These changes are part of the process of cell death. Affected cells are called ischemic neurons or red neurons or eosinophilic neurons.


Case 2

Bacterial meningitis (Neisseria meningiditis aka meningococcus)

  • Multiple lobed nuclei (neutrophils)
  • Macrophages
  • Proteinaceous exudate in subarachnoid space
    • Arachnoid granulations also contribute to the arachnoid eosinophilia
    • -->Fibrinosuppurative exudate in subarachnoid space
  • Clinical effects
    • Headache/pain, stiffness of the neck (reflex spasm of vertebral muscles to prevent stretching of underlying meninges by turning the neck)
    • Fever (TNFa, IL1 and resetting hypothalamic thermostat)
    • Swelling - raise intracranial pressure
      • Decreased level of consciousness, confusion, coma, nausea, vomiting
    • Irritation when looking at bright light (photophobia)
  • Most of the organisms that cause meningitis come from the nasopharynx (spread via bloodstream)
  • Fatal consequences:
    • Septic shock
    • Raised intracranial pressure
      • Herniation syndromes
  • Diagnosis
    • Lumbar puncture (between L3/L4 vertebrae - spinal cord ends at L1/L2) and take a sample of CSF
    • Manometer should show 5-15cm water if healthy. Pressure should be increased in meningitis
    • CSF appears purulent/cloudy due to neutrophils in subarachnoid space
  • Usually, only a few mononuclear cells are resident in the subarachnoid space and no red cells or neutrophils. The cells you would see in pathology is neutrophils. Any neutrophils in the subarachnoid space are abnormal - indicating pyogenic infection of the CSF
    • Urgent gram stain needed
      • Gram Neg Cocci = meningococcus
      • Gram Pos Cocci = streptococci
  • CSF glucose would be low due to bacteria in CSF utilising glucose OR metabolism of glucose by neutrophils and by increased usage of glucose by underlying tissue.
  • Proteinaceous exudate causes increase in CSF protein levels
  • Results differ between viral and bacterial meningitis (viral is actually more common)
    • Look up the differences in CSF test results between bacterial and viral
  • Identify antibiotic sensitivities to treat people.

Labelled slides