Cns
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CNS THEORY
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Transcript of Cns
CNSTHEORY
Anatomy
(sensory ones ) : usually both axons and dendrites are myelinated
Astrocytes can be identified histochemically, so if you are examining a section of nervous tissue and you want to see if it has astrocytes , you can design an antibody against the protein GFAP (glial fibrillary acidic protein). This protein is a MARKER for astrocytes.
ASRTOCYTE
It is a challenge to make the drug for a brain disease passing the BBB when this drug aims to. Under physiological conditions, sometimes it is difficult. For example, in Parkinson's disease which results from dopamine shortage, you think that we simply have to give dopamine , but actually dopamine cannot cross the BBB, so they needed to find a drug similar to dopamine called L-dopa that can cross the BBB.
For the somatic nervous system we have one neuron carrying the message. The autonomic nervous system is two neurons chain, preganglionic and postganglionic .
There is a small fissure between the cerebellar hemispheres, but not as deep asFalxCerebri, called Falx Cerebelli
Cerebrum: composed of right and left cerebral hemispheres and separated by longitudinal cerebral fissure and connected by corpus callosum.
Second one to delineate occipital lobe
There is another 2 gyri in the inferior surface, one is called occipito-temporal gyrus and the other is called parahippocampal gyrus and between them there is a sulcus called collateral sulcus.
The most anterior part of the parahippocampal gyrus is actually a special structure called the uncus.
The inferior aspect of the frontal lobe have the olfactory tract travelling, medial to the olfactory tract there is a gyrus called gyrus rectus, and lateral to the olfactory tract there is orbital gyri, the separation between the two gyri is the olfactory tract or the olfactory sulcus which is beneath the olfactory tract.
Claustrum : thin line of grey matter / its function isn't well known
septum pellucidum (double membrane) : delicate membrane(you can tear it and find a space “part of anterior horn of lateral ventricle” ) that bounded by corpus callosum superiorly and fornix (bundles of fibers that originate from hippocampus ) inferiorly .
*Cistern: Any opening in the subarachnoid space of the brain created by a separation of the arachnoid and pia mater. These spaces are filled with CSF
*Location:-Superior parietal lobule.(brodmann areas 5, 7).
❺Motor cortex : in frontal lobe .Primary motor cortex:responsible for executing the movement in the contalateral part of the body .-Precentral gyrus (lateral)-Anterior part of paracentral lobule (medial)
•Secondary motor cortex:responsible for coordinating (integrating ) sensory input ,to allow the sensory input to influence the movement /also responsible for programming skilled movement .16*We have :- One in the lateral surface called " premotor area " .- One in the medial surface called " supplementary motor area " . -Lateral aspect of frontal lobe
SPINAL CORD SEGMENTSWe have: 8 cervical segments 12 thoracic segments 5 lumbar segments 5 sacral segments 1 coccygeal segmentThe same numbers for the spinal nerves as well.
1. Cervical Enlargement: C4 – T1 Provide brachial pluxse2. Lumbar enlargement: L2 – S3
These enlargements are caused by the large numbers of neurons present in those areas
L2 – S3
- Before the level of S2, The filum terminale (internum) is only made up of Pia Mater and some neuroplial cells. After S2, the dura mater terminates and becomes a thread like structure that covers the Filum terminale and now we’ll have theFilum terminale externum.
- Filum terminale externum is also known as Coccygeal ligament.
-If the attachment of the filum terminale is at the wrong place (due to developmental deformity), it will result in major neurological deformities.
LUMBAR PUNCTUREThe best position to be in is the lateral recumbent position (fetal position) because it will give maximum distance between each transverse process.
THE FASCICULUS, MEANS: BUNDLE OF AXONS OR BUNDLE OF FIBERS.
So if I examined a section of the spinal cord at the sacral,lumber, OR coccygeal level, we’ll only see the gracile fasciculus of the posterior funiculus.
What about the levels of T5, T1, and C7?!
… Here you will see gracile fasciculus travelling to the brain
medially, lateral to it you will see the cuneate fasciculus. In fact there is no such physical boundary , you will just realize that the posterior fasciculi in the cervical segment are much larger than those in a sacral segment.
VERTEBRAL ARTERY BRANCHES
BASILAR ARTERY BRANCHES1-pontine arteries as the name indicates the will supply the pons2- Labyrinthine artery which is very low compared to other branches of the basilar artery (very long and tortuous- متعرج - artery that will reach the inner ear)3- Anterior inferior cerebellar artery4- Superior cerebellar artery5- Posterior cerebral artery (one of the main arteries of brain) supplies occipital lope of cerebrum laterally and medially
also we have central branches like posterior choroidal artery and thalamogeniculate artery which participate in supplying the internal capsule and the basal nuclei
• Inferio-medial aspect of the temporal lope and most of the thalamus are supplied by posterior cerebral artery(pink)
• Anterior chorroidal artery supplies both chorroid plexus and hippocampus(green
internal cerebral vein is formed at the interventicular foramen by the union of thalamostriate vein (thalamus / caudate and putamen part of basal nuclei) and Choroidal vein
CORTICOSPINAL
The anterior corticospinal spinal will have the same origin as lateral corticospinal , travel in the same regions until we reach the caudal part(most inferior part) of medulla at this point the lateral corticospinal tract will cross the midline and will start traveling in the lateral funiculus whereas the anterior corticospinal tract won't cross the midline it will continue traveling in the anterior funiculus and it will cross the midline in the spinal cord
anterior corticospinal tract responsible for supplying the trunk and neck muscles , so mostly this tract will be limited to the cervical segments of the spinal cord .
MEDULLA OBLONGATA AT THE LEVEL OF DECUSSATION OF PYRAMIDS
In this pic the decussation of the pyramid occurs at the caudal part of medulla oblongata
AT LEVEL OF DECUSSATION OF LEMINISCI
PONS AT LEVEL OF TRIGEMINAL NUCLEI (THROUGH CRANIAL PART)
LATERAL LEMINSCUS- Nothing to do with
medulla - In the midbrain ,it will
appear in the inferior section.
http://www.neuroanatomy.ca/flex_labs/BrainstemOverview/story.html
MIDBRAIN: THROUGH INFERIOR COLLICULI
frontal
cortex
temporal
circle of Willis is located in the interpeduncular fossa of the midbrain
MIDBRAIN: THROUGH SUPERIOR COLLICULI
accessory
RED NUCLEUS
# In the spinal cord, there is no fibers/bundles for the face because your face is supplied by cranial nerves not spinal nerves. So below the brain stem there is no more fibers for our face.
Normal 3 years old child will have babinski sign; because much of his/her axons in the CNS are still unmyelinated /immature
INDIRECT PATHWAYS (EXTRA-PYRAMIDAL1-The reticulospinal tract (cortico-reticlospinal tract) => originate in the brainstem(scattered neurons called reticular formation) and end in the spinal cord. It facilitate or inhibit voluntary muscle activity depend on planned movement you are trying to do and it is subjected to your conscious control.
4-The vstibulo-spinal tract => arise from the vestibular nuclei, the tracts maintain our balance and posture . It inhibit Flexor muscles and facilitate the extensor muscles. because the stand position is done by extension of the lower limb . [ this tract receives Input from both the cerebellum and the inner ear to modify movement ].
( lemniscal pathway)
First order neurons: start from sacral segment and go up until reaching the cervical segments.These First order fibers will be arranged from medial to lateral ,so the sacral fibers will be most medial in each funiculus of the spinal cord then coccygeal then lumber..etc!
2nd order fibers are calledDuring crossing :- Internal arcuate fibersAfter crossing and crossing to the brainstem :- Medial lemniscus
Spinocerebellar tracts
CEREBELLUM
PEDUNCLES
dens
Physiology
ROLES OF ASTROCYTES IN BLOOD FLOW CONTROL
Autoregulation maintains CBF between a CPP range of approximately 50 - 150 mmHg
Outside these ranges CBF becomes pressure-dependent
Above 150 mm Hg: blood flow increases with increasing pressure, but most importantly, the blood vessels begin to stretch. This stretch can lead to damage and eventual rupture (stroke). Less than 20ml/100g/min >>considered to be ischemic threshold
HOW CSF ABSORPTION OCCUR: Cells of the villus membrane may actively form vacuoles that transport fluid from one side of the cell to the other.
-CSF absorption is passive and is dependent on higher CSF hydrostatic pressure than venous blood Flowing into the blood
Normal pressure in the CSF system when one is lying in a horizontal position averages 130 mm H2O
Rate of CSF formation is constant while rate of absorption is under regulation.
Increased ICP leads to loss of CSF and reduction in venous volume to compensate for increases in brain volume.
High ICP causes herniation of brain, distortion and pressure on cranial nerves as well as vital neurological centers.
Any trauma will cause an increase ICP>> lead to venous compression >>then increase hydrostatic capillary P that will cause edema
Thalamus is a relay station which means all types of sensation (except olfactory4) have to pass through the thalamus.
Facial recognition area is found on the medial undersides of both occipital lobes and extends to medioventral surfaces of the temporal lobes.
SPATIAL NEGLECT
It’s the inability of a person to process and perceive stimuli on one side of the body (patients neglecting their own contralesional body parts)7 and it is not due to a lack of sensation.
Speech involves two things:1. Formation in the mind of thoughts to be expressed and the choice of words.
The ability to store certain words, know their meaning, pick the right word, or analyze the meaning of a heard or seen word is considered sensory part of communication. (That’s why when this is affected we’ll call it sensory aphasia). controled by Wernicke area2. Motor control of vocalization and the act of vocalization.
The motor coordination required for speech. controled by Broca area.
Neurons in “memory” pathways (which are paved) were arranged in reverberating circuits (a closed circuit; trying to keep the information within).
Molecular basis for memory:Transmitter (serotonin) activates G protein which in turn activates adenylate cyclase resulting in an increase in cAMP.
cAMP activates a protein kinase that phosphorylates a component of the K+ channel blocking its activity.
Blocking K+ causes depolarization. prolongs the action potential which increases transmitter release. This is the basis of positive memory (facilitation of memory).
Long term memory:-It results from a structural change (permenant) in the synapse which is an increase in the area for vesicular release therefore more transmitter is released.
-During periods of inactivity the area decreases in size. (a practical advice based on this would be not retiring early to keep using your brain in oreder not to developing alzhimer’s disease).
Brain Centers for Memory1. HippocampusIt’s critical for long-term memory.
It’s involved in determining which sensory experiences are important and which do not require attention.
2. ThalamusThalamic structures are important for learning and recalling memories.
HIPPOCAMPUS • Originated as part of the olfactory cortex.
• In animals the sense of smell is an important determinant of behavior (is it good to eat, does it smell like danger, is it sexually inviting).
• Role in initiating behavioral reactions such as pleasure, rage, passivity, or excess sex drive.
Excitatory Signals from the Brainstem Bulboreticular facilitory area:
Sends excitatory signals to the antigravity muscles1.
Sends excitatory signals to the thalamus and from here they are distributed to widespread areas of the cortex.
NEUROHORMONAL CONTROL OF BRAIN ACTIVITY
LIMBIC SYSTEM
The HIPPOCAMPUS is the main input; the HYPOTHALAMUS is the main output.
REWARD CENTERS Stronger stimuli can cause rage (intense form of anger), You have to deal with moderate stimulation to stimulate reward !
Less potent reward centers (secondary) are found in the septum, the amygdala, certain areas of the thalamus and basal ganglia, and extending downward into the basal tegmentum of the mesencephalon.
DOPAMINE CIRCUIT.
- The reward circuitry underlying addictive behavior includes amygdala and nucleus accumbens (Ventral Striatum ).
- The amygdale plays a central role in cue-induced relapse. The pathway of motivated behavior involves the prefrontal cortex, the ventral tegmental area, the amygdale, the nucleus accumbens and the ventral pallidum.
- This pathway is involved in the motivation to take drugs of abuse (drug-seeking) and the compulsive nature of drug taking.
- The VTA activates the NAs (nucleus accumbens), which produces a pleasurable feeling. The activation of the NAs causes the release of dopamine.
Norepinephrine (NE) :- Mainly it is in the ventral tegmental area (VTA) and substantia nigra
Stimulation in these areas causes the animal to show all the signs of displeasure, fear, terror, pain, punishment, and even sickness.
Stimulation of punishment centers can inhibit the reward centers completely, i.e., punishment and fear can take precedence over pleasure and reward.
AMYGDALA
• Receives input from other areas of limbic system as well as most areas of the cortex.
Sends output back to cortex as well as into hippocampus, septum, and hypothalamus
Functions in behavioral awareness at the semiconscious level.
• it determines the person’s surroundings.
• Helps pattern behavior appropriate for the each occasion.(v.imp) It’s very important, destroying it leads to inappropriate behavior.
if both amygdalae were destroyed under extreme conditions, this will result in Klüver-Bucy Syndrome, this occurs only in animals; but we study it to understand the importance of amygdala.
situated in the temporal lobe
Males tolerate pain MORE than females. To have a better survival chance, we don't have to tolerate pain (we have to feel the pain)! Females are MORE important for survival for humanity.
* Noxious stimuli: stimuli that elicit tissue damage and activate nociceptors.
Nociceptors Distribution:— - Superficial layers of the skin, certain internal tissues; periosteum, arterial walls, joint surfaces, falx (fold in dura mater) and tentorium in the cranial vault, & visceral organs.
- The cell bodies of nociceptors are mainly in the dorsal root and trigeminal ganglia (all over the spinal cord).
Globulin and protein kinases. It has been suggested that damaged tissue releases globulin and protein kinases, which are believed to be amongst the most active pain-producing substances. Minute subcutaneous injections of globulin induce severe pain.
NGF then binds to TrkA receptors on the surfaces of nociceptors leading to their activation.
Substance P (SP) and calcitonin gene-related peptide (CGRP)
prostaglandins block the potassium efflux released from nociceptors following damage, which results in additional depolarization. This makes the nociceptors more sensitive. Aspirin is an effective pain killer because it blocks the conversion of arachidonic acid to prostaglandin.
Reticular formation: activate cerebral cortex and maintain wakefullnes.• Composed of Gray +white matter• Connected with intralaminar nucli of
thalamus• When ascending fibers decrease throw
reticular formation >> going to sleep
Fibers arising from the intra laminar nuclei of the thalamus, thalamocortical fibers.
SUBSTANCE P
• Thought to mediate lower back pain, arthritis, fibromyalgia.
• Over-the-counter , OTC drugs containing capsaicin (made from chili peppers) can deplete Substance P from local nerve endings and relieve pain.
Feeling pain: Pain transmitted from periphery go to spinal cord, Nociceptor ( Pain receptor). It synapsis with second ordered neuron that cell bodies’ in the spinal cord go up toward the thalamus, from the thalamus its synapsis again and go to the cortex through the third ordered neuron and once it reaches the cortex then you can feel the pain.
NATURAL PAIN SUPPRESSION ("ANALGESIA")• 1- The PAG and periventricular nuclei (release β-endorphin).
• areas in the hypothalamus excite the PAG area can also suppress pain
2. Raphe magnus nucleus → release serotonin → serotonin enhances the area in the spinal cord to release encephalin (endorphin )
3. Pain inhibitory complex -Descending pathway- located in the dorsal horns of the spinal cord (dorsolateral funiculus)→releases β-endorphin;regulates spinal inhibitory complex.
— Dorsolateral funiculus is comprised of
i. serotonergic (5-HT) fibers nucleus (raphe magnus)
ii. dopaminergic neurons from ventral tegmental area
iii. adrenergic neurons from the locus coeruleus
** Imaging studies: Placebo administration with expectation of an analgesic agent is associated with activation of opioid receptors in cortical and subcortical regions that are part of pain control system.
Origin of Brain Waves - is summation of neurons in the same direction and polarity
ALPHA WAVES
stimulation in the nonspecific layer of reticular nuclei that surround the thalamus or in “diffuse” nuclei deep inside the thalamus often sets up electrical waves in the thalamocortical system at a frequency of 12 per second, which is the natural frequency of the alpha waves.
Focal seizures can spread locally from a focus or more, to the contralateral cortex and subcortical areas of the brain through projections to the thalamus, which has widespread connections to both hemispheres.
PHARMACOLOGY
psychosis:
patient with psychosis, the theory says that “there is a lot of dopamine in the system compared to glutamate” (so for a pharmacological intervention we think about blocking the excess dopamine)
NMDA receptors are for glutamate, so if you block glutamate, dopamine levels increase compared to glutamate.
Discontinuation syndrome: (when you stop taking the drug)
Headache, malaise, nervousness, sleep disturbances.
More with short acting drugs.
Fluoxetine is the safest.
LITHIUM
only used in status epilepticus if all other options such as benzodiazepine, phenytoin, fosphenytoin and valproic acid failed to produce stabilization of the patient
Phenobarbital
MOA OF OPIOID RECEPTOR
OPIOID
BDZ OVERDOSE
Pathology
REACTIONS OF COMPONENTS TO INJURY: NEURONS Acute
REACTIONS OF COMPONENTS TO INJURY:ASTROCYTE
INCREASED INTRACRANIAL PRESSURE:
TONSILLAR HERNIATION
http://www.neuroanatomy.ca/flex_labs/Herniation/story.html
CAUSES OF INCREASED ICP:
CONGENITAL MALFORMATION
CVA
GLOBAL HYPOXIA
in patients with cardiac problems and need CPR but this CPR is ineffective.
INFARCTION (FOCAL ISCHEMIA)
Lots of astrocytes & few macrophages means a lesion that is many weeks or months old A lesion with sheets of macrophages & relatively few reactive astrocytes is 1-2 weeks old
HYPERTENSIVE CEREBROVASCULAR DISEASE
3- vasculitisassociatedhemorrhage, whether its inflammatory, like syphilis, TB, aspergillosis, CMV, whether primary angiitis of the CNS or autoimmune mediated like arthritis nodosa
yellow because its old hemorrhage
don’t have any brain tissue in-between
Microbiology
MENENGITIS
Meningism which is basically a triad of
1. Headaches.
2. Nucal stiffness (neck stiffness).
3. Altered sensorium (meningoencephalitis).
TB Meningitis It usually causes chronic meningitis
To detect it we use a Ziehl–Neelsen stain followed by a lowenstein Jensen medium culture for isolation of TB (
takes 6 weeks to get the results) or PCR polymerase chain reaction-.
PPD test,
TB
VIRAL MENINGITIS
CHRONIC MENINGITIS
