Cerebral Cortex Lecture Flashcards
Cerebral Cortex: 2 categories of layers
1) Supragranular layer
- layers 1-4
- last to develop
- associational fibers-neurons talking to neurons on same side of brain
2) Infragranular Layer
- Layers 5 & 6
- commissural fibbers (neurons that communicate to other side of brain)
Golgi Stain
- Silver strain
- neurons, axons, and dendrites
Nissl stain
1) all cells in brain
- Nissl Bodies (ReR)
Weigert Stain
Myelin Stain
-myelinated axons
Layers of Cerebral cortex
1) Molecular Layer
2) External Granular Layer
3) External Pyramidal Layer
4) Internal Granular Layer
5) Ganglionic Layer (internal pyramidal layer)
6) Multiform layer (layer of polymorphic cells)
- many different types of neurons and microfilm
- many astrocytes and oligoendroglia (satellite cells)
- Blood supply from pail surface
Hippocampal Cortex
Has only 3 layers
1) Molecular
2) Pyramidal
3) Polymorphic
Blood Brain Barrier
1) Capillaries are tight, do not leak
2) Blood is toxic to CNS tissue
3) Endothelial cells bound tightly to capillaries via tight junctions to create BBB
- water, gases, and lipid soluble small molecules can diffuse across endothelial cells
- other substances=transport systems-highly selective
4) Brain bleed=toxins pouring into head-» kills brain cells
* *Protects neurons from direct exposure to tissue fluids
Excitotoxicity
Increase in excitatory Neurotransmitters=Kills neurons
Glutamate
1) Excitatory Neurotransmitter
- causes neuron action potentials
2) Plasma is loaded with glutamate
- brain bleed= excitotoxity
- causing the neurons to overexcite and kill them
3) BBB KEEPS FROM CNS
Glial vs neurons
10: 1 glial to neurons
- most brain tissue is made of glial cells not neurons
Cortical Cell types
1) Pyramidal Cells
2) Betz Cells
3) non-pyramidal cells (aka interneurons/internuncial neurons)
Pyramidal Cells of cerebral cortex
1) Excitatory
- ex: Glutamate
2) Found in all layers EXCEPT layer 1
- mostly found in layers 3 & 5
- cells in layer 2/3 give rise to associational fibers
- cells in layer 4, project to thalamus
- layer 5-project to anterior (Ventral) horn of the spinal cord, brain stem, thalamus, basal nuclei, other regions of cortex.
- AXONS from these cells going to spinal cord form=CORTICOSPINAL TRACTS
- layer 6- project to thalamus and cortex
Betz Cells of cerebral cortex
1) Very large Pyramidal Cells
2) Found only in layers 5 of precentral gyrus
- projects to the lumbar spinal cord
- control leg movement
Non-pyramidal Cells of cerebral cortex
Aka interneurons or internuncial neurons
-function as local circuits (talk to neurons in area=short axons)
4 types of cells-receive excitatory input from the thalamus
1) Spiny stellate cells
- excitatory
- layer 4
- projects to other columns
2) Aspiny stellate cells
- inhibitory
- layer 4
- projects to other columns
3) Basket cells
- inhibitory
- all layers
- projects to other columns
4) Chandelier Cells
- inhibitory
- layer 3
- projects to Pyramidal cells within a column
- may be involved in schizophrenia, by not doing its job
Inhibitory Neurons
1) use GABA (game-aminobutyric acid) to systems=become overactive
Afferent projections to the cortex from lower centers
-think thalamus
1) Ventral lateral nucleus of thalamus
- motor cortex
- layer 3 and 4
2) Specific afferent projections- moving toward cortex
- layers 3 and 4
- lateral geniculate projects toward visual cortex
- medial geniculate projects toward auditory
- ventral posterior nucleus of thalamus projects to pain and temps
3) Nonspecific afferent projections
- Lateral dorsal nucleus
- Pulvinar nucleus
- Reticular Nucleus
- mostly layers 1 and 2
Projection
1) axons carrying impulses from the cortex to lower centers or from lower centers to the cortex
Association efferent
Interconnecting different regions of the cortex of the SAME SIDE OF THE BRAIN
Commissural Efferents
Interconnecting similar regions of the cortex on the OPPOSITE SIDES OF THE BRAIN
-ex: Corpus Callosum, ANt commissure
MAturation of major neural tracts and cortical areas for reflexes/behavior
Pattern of myelination-when your fully developed tract
1) spinal reflex
- fetal months to 2 months old
2) Motor control
- ending of fetal months-> 2-4 y.o.
3) Sensory
- fetal months-> 2/3 y.o. (Motor a little longer)
4) Behavior
- birth-> early 20’s
5) Judgement and reason
- 3 y.o.-> rests of life
Myelination of fibers
Myelin allows for faster signal down axon
-myelination is a gradual process
Prefrontal Cortex
-Brodmanns areas
Areas 9,10, 11, 12
- judgement
- reasoning
- personality
- working memory (temporary)
- motivation
Male vs female cerebral cortex
Females cerebral cortex= 19 billion neurons
Male cerebral cortex= 23 billion neurons
Developmental Neuro
1) at 100 days basic parts are there
2) a 7months start developing gyri
3) at 9 months=fully developed
- no new neurons are added after birth
- 73,000 miles of myelinated tracts
- lose 30% of myelinated tracts as you get older
as you get older-> same number of neurons but different levels of complexity w/age
- more enrichment=more complexity of dendrites
- Dr. B less complex dendrites with less spines (coming off of dendrites)
Muscle Spindles
Intramural fibers
-sensory fibers that tell CNS what skeletal muscles are doing
Cerebral localization-Penfield Homunculus
1) Postcentral Gyrus=SENSORY CORTEX
- middle cerebral artery supplies Upper Extremity and Face (lips, tongue, teeth, pharynx)
- ANterior Cerebral artery supplies Lower Extremity and Head/neck
2) Precentral Gyrus= MOTOR CORTEX
- Middle cerebral artery supplies Hand and Face (lips, tongue, swallowing)
- Anterior Cerebral artery supplies Upper and Lower extremity (minus Face and Hands)
Apraxia
1) Inability to perform a a purposeful movement w/out paralysis
2) disorder of motor control
- may occur after damage in parietal association cortex, premotor cortex, or supplementary motor cortex
3) May affect the muscles of speech
- seperate disorder from aphasia
Brodman’s Area for Post Central Gyrus
Primary Sensory Cortex (S1)
Post central gyrus
3a-Propioception (aware of body parts in space) from muscle spindles
3b+1->-cutaneous afferent
2- Golgi tendon organ and joint afferent
S1
Primary Somatosensory cortex
- post central gyrus
- Brodmanns area 1,2,3
- 3a=propioception from muscle spindles
- 2-golgi tendon organs and joint afferents
- 1+ 3b= cutaneous afferents
M1
Primary Motor Cortex (M1)
- Brodmans Area 4
- Precentral Gyrus (right Half)
Broca’s area
Brodmanns ares 44 and 45 of Left Brain
- inferior frontal gyrus
- speaking and writing language
Broca’s Aphasia
Lesions of Frontal inferior gyrus Broca’s area 44 and 45 of Left brain
AKA expressive aphasia or nonfluent aphasia
1) Able to comprehend language but can’t speak fluently (can’t express themselves)
- Not paralysis of vocal aparatus
- difficulty writing (agraphia) but they can understand written language (read)
2) most common causes:
- tumors/occlusion of- frontal M4 branches of middle cerebral artery
3) other Symptoms-contralateral motor signs and symptoms such as
- weakness (paresis) of the lower part of face
- weakness of the arm
- motor weaknesses + aphasia=occlusion of branches from the proximal parts of the middle cerebral artery (M1) including lenticulostriate arteries
4) Full-blown brocas aphasia
- doesn’t affect just brocas area-> includes insular cortex and white matter
5) Severe Brocas aphasia
- unable to speak=mutism
- still understand speech, can swallow and breathe normally
6) Less severe case
- limited speech is possible
- short habitual phrases such as “Hi, fine, thank you, and yes or no are the first to come back
7) Mild Broca aphasia
- damage only affects cortical area
Brodmanns area 5
To the Right of postcentral sulcus/gyrus
Sensory association
Wernickes area
Brodmanns areas:
- 39=written
- 40=connecting
- 22=spoken (sometimes)
Language center
- left side of brain
- comprehend spoken or written language
Visual Cortex
-Brodmanns areas
17, 18, 19
- more complex moving towards 19 (inner) from occipital pole
- 17=light patterns
Brodmanns area 21
Higher order visual audio memories
- middle temporal gyrus
- memories and language
Heschls gyrus
Brodmann areas-41 and 41
- Primary Auditory Cortex
- process what is heard
Brodman’s Area 43
Primary Gustatory Center
- Located below central sulcus above Sylvian fissure
- dysgeusia (gustatory illusions)
Brodmanns areas 7
Parietal Eye field
-eye movement
Brodmanns Area 6
1) Premotor cortex
2) Supplemental motor cortex (M2)
Achromatopsia
Damage up area 19 of visual cortex
- has to be bilateral
- no color seen or able to imagine
Akinotopria
- lesion along inferior temporal sulcus
- cannot perceive motion
Brodmanns area M3
Cingulate Sulcus
-medial view
Brodmanns area S2
Medial view
- deep within central sulcus
- receives input from S1
- has strong connection with amygdala and Hippocampus
Brodmanns area 34 and 36
Medial view
- recognizing faces
- parahippocampal gyrus
- read emotions on someone’s face
Brodmanns area 20
Inferior Temporal Gyrus
-higher order visual memories
Brodmanns 37
Inferior Temporal Gyrus
-higher order visual processing
Premotor Cortex
- function
- lesion
Premotor Cortex
- voluntary motor function that is dependent on sensory input
- ex: reaching for object in space
- involved in planning and executing movements
- approx 30% of pyramidal fibers are from here
- has strong projections to primary motor cortex (area 4)
- receives input from the supplementary motor cortex
Lesion:
- causes apraxia=cannot perform purposeful movement in the absence of paralysis
- pt has difficulty walking and performing other complex motor tasks
Supplementary Motor area
Aka (M2)
- approximately 5% of pyramidal fibers
- involved in planning movement (rather than executing movements)
- activated when pt asked to flex multiple fingers in a SPECIFIC sequence (along with m1)
- Mental reps (not actually doing reps)
Area 5 and 7-non dominant hemisphere
- function
- lesion
Personal Geography
- knowledge of where you are in enviroment
- knowledge that your body parts are yours (angular gyrus involved-area 39)
Lesion:
- cannot learn a new enviroment
- may deny a body part is yours or neglect it
Hemineglect
1)aka contralateral neglect
2) damage to the right parietal association cortex (nondominant)
-pts will be unaware of objects and events in the left half of his/her surrounds
3) Milder forms:
-tendency to ignore things on the left side of the patients surroundings
4) Extreme cases
-don’t even recognize the left side of his or her won body (ASOMATOGNOSIA)
-ex: ignore left side when dressing
5) other symptoms:
-losing the ability to function successfully within spatial surroundings
-ex:unable to describe his/her route on the way home from work
-unable to manipulate objects in space (contraction always apraxia)
Ex: legos
Area 39 and 40-non dominant hemisphere
- function
- lesion
1) Rhythm and feeling into speech
- the way one says words
- interpreting the emotional tone of the speech of another person
2) Lesion
- cannot sing
Area 22-Nondominant hemisphere
-function
Comprehending voice inflections (pitch/tone)
Right vs Left brain:
Right:
- creative (mostly)
- can-simple quantitative functions (summing small integers)
- can understand simple language
Left:
- Language
- Verbal
- Analytical
- quantitative
- Linear (mostly)
Anosognosia
1) Inability to acknowledge disease in oneself
2) ONLY RIGHT brain stroke-insular cortex and S1 and S2 + motor cortex= L side paralysis
- pts tend to have anosognosia
- Right side S1, S2 and insular cortex=centers for integration of body awareness
3) Left brain stroke-same area=no anosognosia
- have issues with social interaction and personal decisions
Right side S1, S2 and insular cortex
Centers for integration of body awareness
Corpus Callosum
Larger in females than males
ACC
AGENESIS OF CORPUS CALLOSUM
- doesn’t develop at all
- doesn’t hinder person much
Hypoplastic Corpus Callosum
-underdeveloped corpus callosum
Lissencephaly
- Smooth brain
- no gyri or sulci developed
- vary degrees of severity
- live 1-2 years at most
- caused by: genetic or viral infection during pregnancy
Visual Fields to Visual Cortex
1) Each eye talks to both visual cortices
2) Visual fields are lateralized, not eyes
Sodium Amytal test
Aka Wade Test
1) Inject a barbiturate (drug-shuts down activity) into R or L internal carotid Artery
- determines which hemisphere is dominant for speech function
- avoids neurosurgical procedures that might destroy language ability
2) Pt asked to count backwards will being injected
- Hemisphere dominant for speech is affected= pt stops speaking and does not respond to a command to a command to continue
3) Test revealed that:
- 96% of Right handed people are L brain dominant for speech
- 70% of L handed people are L brain dominant for speech
- 15% of L handed people control of speech in both hemispheres (injection didn’t supress speech fxn)
- suppressing L hemisphere produces brief depression feeling
- suppressing R hemisphere produces brief feeling of euphoria (buzz)
- Functions related to MOOD may be lateralized in brain
- Smage w/ R hemisphere-pathological indifference to their disability
Split Brain Experiments
1) Epileptics
- provided hemisphere function
- prevent seizures from spreading from one side of the brain to other=cut the corpus callosum and anterior commisure
- each hemisphere can function independently
- R-generally mute and cannot communicate about its experience verbally ; can do many things of L
- Sensory analysis, memory, learning, and calculation performed by each hemisphere (R limited)
2) Split Brain patients
- function normally
- both hemispheres receive information from the world bc of the crossing pattern of visual input
Split Brain patient- Right side removed; apple experiment
1) Shown apple in right visual field
- projects only to left hemisphere visual cortex
- sees object
2) Shown apple in L visual field
- pt denies seeing anything
- if brain doesn’t know why you did something, it will manufacture a reason yo will believe is true
Memories
- reconstruction of fragmented parts
- assembling wrong=false memory (feels right)
- ego edits memories to make us remember them how we want to remember them
Microglia
1) like macrophages-phagocytic
- predominant cells involved in CNS inflammation
2) secrete IL-1B, TNF-a, prostaglandins, and neurotoxic molecules (glutamate, oxygen radicals)
- secondary cause of neuronal damage following trauma or stroke
HIV
targets microglial in the CNS
-leads to neuronal damage and dementia
Wernickes Aphasia
1) AKA receptive or fluent aphasia
2) defect of the comprehension rather than expression of language
3) Cause:
- occlusion of temporal and parietal M4 branches of the middle cerebral artery
- hemorrhage/tumors into thalamus extending laterally and caudally to invade the subcortical white matter
5) Severe wernickes aphasia
- unable to understand what is said to them
- unable to read (Alexia)
- unable to write (agraphia)
- fluent paraphasic speech (can talk normally)
- unintelligible bc of frequent errors of word choice or made-up words
7) less severe cases
- paraphasias occur:
- literal paraphasia (incorrect but similar sounding word),
- verbal paraphasia (word seems appropriate to the patient but is incorrect)
8) Much less aware of the extent of their disability vs patients with Broca’s
9) Damage to basal nuclei-> associated with language disorders similar to wernickes
Damage to basal Nuclei
Associated with language disorders similar to wernickes
Agnosia
1) Disorder of sensory perception
- not a loss of primary sensation (touch, vision, hearing)
- Loss of the ability to interpret the sensation
2) only one sensory modality
3) difficulty in recognizing complex sensory stimuli
4) Forebrain lesion may cause variety
Visual Agnosia
Inability to recognize a familiar object by sight
Somatosensory agnosia
inability to recognize a common objects such as a coin, pencil, or key using sense of touch alone (tactile agnosia, asterognosis)
Olfactory Agnosia
deficits to sense of smell
Gustatory agnosia
Deficit to sense of taste
Color Agnosia
Inability to recognize colors
Hippocampus
- Involved in memory (declarative)
- bilateral-in temporal lobes
- strong connection with S2 (along with amygdala)
Amygdala
- responsible for base emotion (rage, anger, sexual)
- limbic system
- emotion valence driven by Amygdala
- temporal lobe
- strong connection with S2 (along with hippocampus)
Written/spoken/and hearing language
1) NOt wired for written language
- only hearing and speaking language
Pidgin
Melding of 2 languages
- 2 come together to 1
- basic grammatical structure
Creole
1) new language with grammatical complexity
- arose from pidgin
- comes from children
Angular Gyrus
-dominant hemisphere
1) strong connection with Vision, language, and auditory areas
2) working with numbers
- quantitative ability
3) interpretation of symbols (letters)
Arcuate Fasciculus
1) allows wercicke’s and brocas to communicate
- conduction aphasia
- dominant hemisphere (L)
Lesion on temporal Pole results in:
1) Anoia
- trouble remember proper names
Superior Frontal Gyrus
-dominant hemisphere
Selfwareness
Middle Frontal Gyrus
-dominant hemisphere
1) Doral Lateral prefrontal cortex
- working memory (temporary)
Left brain vs Right brain
1) Left
- language
- verbal
- analytical
- quantitative
- linear (mostly)
2) RIght
- creative (mostly)
Phonetic symbols and ideographs
1) different parts of the cortex
2) Japanese language
- Katakana-phoentic based
- kanji -ideogram based
Alexia
cannot comprehend written language
Dyslexia
1) may be problem with angular gyrus
2) can read ideogram base language much better than phonetic based language
3) Intelligence is not altered
Synasthesia
atypical modality crossing
-taste something-hear sounds
or see something that causes them to experience colors
Damage to MII, MIII and anterior cingulate gyrus
MIII=deep in cingulate gyrus
Completely mute
- no emotion affect
- sit still (not paralyzed)
- just sits and stares
When they come out:
- will remember everything
- from their perspective they were aware, just did not feel like doing anything
Frontal Lobe
- functions
- lesion
1) Integrates with limbic system
2) appropriate emotional response
- emotion meets behavior (filter)
3) impulse
- EtOH suppresses impulse control
4) Social interaction
5) project oneself into future
6) Lesion:
- delusions, schizophrenia, paranoid
ACG w/DLPFC
Anterior Cingulate gyrus
Dorsal Lateral Prefrontal cortex (middle frontal gyrus)
regulates attention and inattention
VMA
Ventromedial Area
1) Damage
- reasoning and decision making in personal or social decisions
Damage DLPFC
Dorsal Lateral Prefrontal Cortex
-middle frontal gyrus
Damage
- impairment w/abstract reasoning and problem solving
- attention issues
- working memory
Brodmanns area 8
Frontal Eye field
Cytoarchitecture of cortex:
1) Differs from one area to another in ways they are related to function
2) Heterotypical granular cortex
- found in primary sensory cortex
- layer 4-major input layer is thick
- layer 5-major projection layer is narrow and indistinct
3) Heterotypical agranular cortex
- found in primary motor cortex
- layer 4- major input layer-invisible
- layer 5-major projection layer-thick, merges w/Layer 2
4) Homotypical cortex
- all 6 layers w/equal thickness
- found in areas of the neocortex
Higher Cortical Functions of cerebral cortex
Higher intellectual functions
4 functional categories
1) Sensory
-except olfaction
-receive thalamocortical (thalamus to cortex) fibers from diencephalic(thalamus + hypothalamus) relay nuclei related to each modality
A) Primary somatosensory cortex (areas 1,2,3)
-receive projections from ventral posterior (pain and temp) complex of thalamus
-projects to area 5 (sensory association)
B) Primary visual Cortex (Area 17)
-receive projections from lateral geniculate nucleus
-projects to 18 and 19
C) Primary Auditory Cortex (41 and 42)
-receives projections from medial geniculate nucleus
-projects to 22
2) Unimodal Association cortices:
- adjacent to each primary sensory area
1) Visual Unimodal Association cortices (18, 19, 20, 21, 37)
2) Somatosensory Association cortex (area 5)
3) Auditory association cortex (area 22)
3) Motor
4) Multimodal Association cortex:
- receives info from several sensory modalities and creates a wholistic picture of surroundings
- important for comunicating using language, long range plans, imagine and invention
Dominant Hemisphere
1) Controls Language
2) Majority-Left cerebral dominance
- lesions 95% of cases
3) all right handed invidious and 1/2 of left handed:
- L dominant
Aphasia
1) Disturbance of the compression and formulation of language
- not a disorder of hearing, vision, or motor control
- can affect verbal and nonverbal language
2) some language in Nondominate parietal lobe
- lesion
- difficulty understanding the PROSODY (voice inflections, emotional content that may alter the meaning of spoken sentence)
Conduction Aphasia
1) least common type of aphasia
2) Interuption of the Arcuate Fasciculus which allows wernickes and brocas to communicate
3) comprehension- normal
expression-fluent
-BUT THE patient has difficulty translating what someone has said to them in an appropriate reply
Global Aphasia
1) Occlusion of the left internal carotid artery or most proximal portion of middle cerebral artery (M1) produces damage that messes with both Brocas and wernickes area
2) Loss of language completely
Phineas gage
1) Phineas gage
- railroad worker
- struck by rod beneath L eye and exited through the top of his head
- destroying most of prefrontal cortex=CHANGING PERSONALITY
Symptoms: w/bilateral damage to prefrontal cortex
1) Highly distractible or lack of consistency of purpose
2) Lack of foresight
- can’t anticipate or predict future events on basis of past or present conditions
3) Unusually stubborn
- given advice-> disagree
4) lack ambition
5) Lack sense of responsibility
6) lack sense of social porpriety
Rabies Virus
1) Virus replicates in muscle tissue
2) Then transported retrograde
- to cell bodies of neurons
3) Virus replicates in cel bodies
- taken up by the terminals of adjacent cells
- spreading infection through CNS
- behavioral changes associated
4) Virus travels anterograde to salivary glands and shed virus in saliva
Clostridium Tetani
1) Tetanus toxin transported retrogradely
- Axons (sites of infection)-> neuronal cell bodies
- taken up by terminals of adjacent cells
2) Toxin is diluted as it passes cell to cell
- can still produce neurological deficit
Anterograde
1) AKA orthograde
2) Cell body to terminals
3) Can be classified as
Fast transport (100-400mm/day)
-based on action of protein KINESIN= ATPase->moves macromolecule-containing vesicles and mitochondria along microtubules
Slow transport(~1mm/day)
- carries Structural and metabolic components
- less understood
Retrograde
1) Terminals to Cell bodies
2) Driven by dynein
3) ONLY FAST NO SLOW
4) Allows neurons to respond to molecules
- Ex: Growth factor taken up near axon terminal by PINOCYTOSIS OR RECEPTOR MEDIATED endocytosis
5) Also function in recycling of components of axon terminal
HRP
Enzyme horseradish peroxidase or fluorescent substance
- injected into axon terminals
- transported RETROGRADE (toward cell bodies)
Radioactively labeled amino acids
Radioactively labeled amino acids or HRP
- conjugated to WGA-HRP
- injected into cell bodies
- TRANSPORTED ANTEROGRADE
If the cell body of neuron is destroyed?
Anterograde (wallerian) degeneration
-can be seen with SILVER NITRATE STAIN
Injury to axon?
Results in CHROMATOLYSIS
- changes in cell body;
- cell body swells
- nucleus->eccentric position
- Nissl substance disperses
Pain Stimuli
1) Nociceptors
- Noxious (painful) stimuli
2) Thermorecptors
- temperature changs in skin and viscera
Both mediate pain
-most common complaint in clinical medicine
Synapses
1) 2 morphological categories:
- electrical (electronic)
- chemical-unidirectional; vast majority in mammalian CNS
2) Neurological diseases may alter the function of synapses
Disorders of NT Metabolism
1) Parkinson Disesae
2) Bipolar Disorder
3) Alzheimer Disease
4) Myasthenia gravis
Parkinsons
1) Disorder of NT metabolism
2) Affects dopamine-synthesizing neurons in the SUBSTANTIA NIGRA (area of brainstem)
3) Symptoms due to loss of Dopamine
- Tremor
- inablity to properly control movement
4) Therapy/tx:
- L-dopa Supplements-> increases dopamine synthesisn but loses effectiveness overtime
- Carbidopa-> ihhibits L-aromatic amino acid decarboxylase-> can’t cross BBB-> decreases metabolism of L-dopa in peripheral thus more L-dopa available in CNS for dopamine synthesis
- used with L-Dopa
Bipolar disorder
1) Disorder of NT metabolism
2) affects several million American
3) Caused by imalances in the PHOSPHATIDYLINOSITOL (PI)-linked NT systems
4) Increase in PI turnover- triggered by Ach, Serotonin, NE and histamine receptors subcategories
5) Pathological imbalance of PI turnover may result in mood changes
6)TX:
LITHIUM CARBONATE
-stabliizes PI turnover, thus stabilizing mood
Alzheimer Disease:
1) Disorder of NT metabolism
2) Affecs more than 1 million Americans
3) Definitive diagnosis only made postmortem by microscopic exam of brain tissue
4) Characterized by:
- degeneration of neurons in basal forebrain nuclei
- loss of synapses in the cerebral cortex and hippocampus
- presence of neurofibrillary tangles and senile plaques
5) Terminals from Cholinergic (Ach-releasing) cells in basal forebrain nuclei to cortical cells are lost
6) Activity of Choline acetyltransferase (enzyme responsible for Ach synthesis) in cortex and hippocampus is extremely LOW
7) Other NT sysmtes affected
- especially neuropeptides
Myasthenia gravis
1) Disorder of NT metabolism
2) Involves patients immune system protein antibodies to Nicotinic Ach receptors
- ligand gated channel
- found at synapse between primary motor neurons and skeletal muscle fibers
3) binding of antibodies to receptor results in:
- destruction of neuromuscular junctions which causes muscle weakness
Astrocytes:
Type of GLIAL CELL
1) Protoplasmic astrocytes
- located in gray matter
- differ in shape
2) Fibrous astrocytes:
- located in white matter
- greater content of intermediate filaments
3) BOTH CAN BE A SOURCE OF TUMORS-astrocytomas
4) Tight junctions between astrocyte end feed reinforce BBB
5) Can be stained by GFAP
6) can breakdown glutamine to glutamate
7) Proliferation and/or hypertrophy of astrocytes fill in spaces of debris resulting from destruction of cells in CNS injury
Primary Brain tumors
1) arise from cells that make up the structure of the Brian, spinal cord, and its coverings
Astrocytomas
1) location: adult- cerebrum children- cerebrum, cerebellum, Brain stem 2) most frequently encountered glial cell tumor 3) 4 types Grade I Astrocytoma Grade II Astrocytomas Grade III Astrocytoma Grade 4 astrocytoma -1&2 are slow growing astrocystomas
Grade I Astrocytoma
- uncommon tumor
- grows slowly
- usually arise from fibrillary astrocytes in white matter
- occasionally protoplasmic astrocytes
- may form tumors which contain fluid-filled cysts
Grade II Astrocytes
1) Prominent processes filled with glial filaments
2) infiltrate between myelinated axons in white matter
3) Increasingly cluster around neurons in cortical gray matter
4) Commonly encountered in ADULTS
- may take years before symptoms appear
5) If recurs after surgery-more aggressive->higher grade tumor
Grade III Astrocytomas
1) Aka anaplastic Astrocytoma
2) Enlarge nuclei w/increased density of chromatin
- mitotic figures
- uniform nucleus lost appearance
- increased blood vessel density
- RAPID GROWING MALIGNANT tumors
Grade IV Astrocytomas
1) AKA glioblastoma multiforme (GBM)
- highy malignant tumors
2) Spindled shape;
- elongated nuclei
- mitotic figures
3) can invade leptomeninges (arachnoid and Pia)
4) spread to contralateral hemispheres via corpus callosum
5) Complex neovascular structures and sharp borders between living and dead tumor tissue are common intrinsic features
6) “High grade” tumor is most common astrocytoma in:
- middled aged and elderly adults
7) Survival time-only weeks
Oligodendrocytes
1) White Matter- Myelinate axons
Gray matter- neuron “satellite” cells
2)OLIGODENDROGLIOMAS
-slow growing tumor
-adults=cerebrum
-dark round concentric nuclei, w/clear cytoplasm (fried egg in egg white)
-tumor cells form sheets
3) Located in lobes of brain (vs diencephalon or basal ganglia)
3) Hallmark- enlarge clusters around neurons (Satellitosis) and tumor cells beneath Pia mater
Ependymomas
1) Arise from ependymal cells
-line ventricles of the CNS
2) Seen most frequent in children <5 y.o
3) location:
-Children/Adolescents-younger than 10 =4th ventricle
-Adults= spinal cord-> cervical level**
or in location of caudal equine
4) Less infiltrative than astrocytomas and more easily dissected
5) 5-6% of all glial neoplasms
6) most located in posterior cranial fossa (60-75%)
7) True Rosettes
8) Supratentorial lesion
-hydrocephalus
-seizure
9) Infratentorial Lesion
-nausea and vomitting
-headache
-hydrocephalus
-CN Signs
Lymphomas
1) brain tumors that were Once regarded as arising from microglia
2) bone marrow derived=B-lymphocytes
thymus derived cells=T lymphocytes
3) more frequent in patients who suffer from various states of acquired immunodeficiency
(HIV or Immunodeficiency induced meds after organ transplant)
-Epstein-Barr Virus may play a role
4) Tx successfully with medication or radiation (Some)
5) Reach CNS by breaching BBB
-since Brain doesn’t have any lymphatics
Medulloblastomas
1) Cerebellum
2) Tumor that affects children
- boys x2
3) Primitive Blue Cells(stem cells)
4) Neuroectodermal tumor
- can differentiate
5) Most retain unstrained growth of embryonic cells w/o differentiation
6) Quickly spread along surface of brain and spinal cord
- must be treated aggressively
Benign primary brain tumors
1) Ex: Meningiioma and Schwannoma
- covered by capsule that separate the tumor from surrounding brain
- pushes against brain tissue vs extending fingerlike projections that invade white and grey matter
Metastatic brain tumors
1) Arise from malignant cells that originate outside the nervous system
2) Lung Carncinoma
- most common primary tumor to secondarily involve the brain
3) Breast Carcinoma
- may spread to the dura or brain
4) Prostate Carcinoma
- veins of BATSON’s venous plexus-> spinal cord
Degeneration and Regeneration of neurons
1) Neurons are lost through disease or trauma are not replaced
- EXCEPT olfactory epithelium and hippocampus
2) If axons are damaged but cell bodies remain intact:
- regeneration and return of function can occur in some circumstances
3) Axonal regeneration: Best chance
- periopheral nerve is compressed or crushed BUT NOT SEVERED
Monosynaptic reflex arc consists of:
consists of:
- 2 neurons
- 1 synapse
Muscle Stretch Reflex
1) Monosynaptic reflex arc
- 2 neurons
- 1 synapse
2) Input-> Sensory Fibers-> motor neuron in spinal cord
- axon from motor neuron conducts a signal from the spinal cord to the appropriate skeletal muscle=contracts
3) Involuntary Reflex
4) Ex: Tendon reflex test
Localizing Signs and Localization
1) When trying to fine/localize a lesion:
- CN signs are more helpful (Better localizing sign) than long-tract signs in trying to find the lesion
2) Deficits (motor or sensory) located on the same side of the head head and body signify lesions in the cerebral hemispheres
3) Crossed or alternating deficits
- on one side of the head and on the opposite side of the body indicates a lesion in the brainstem (contralateral to brainstem
4) Deficits of only the body
- lesion in the spinal cord
Brain injury that results in weakness or paralysis of upper extremities localized where?
Localizes only to one cerebral hemisphere or to one side of the side of the brainstem
Clinical exam does not tell us which region of the brain is injured (internal capusule, midbrain, pons,, medulla) or whether to lesions is in the upper portions of the cervical spinal cord
paralysis of upper extremities coupled with partial paralysis of eye movement: Lesion localization
1) localized to the midbrain
- damaged the oculomotor nerve and the corticospinal fibers supplying the UE as they transverse this area
Signs vs symptoms
1) Signs
- different from the normal structure/function
- observed and evaluated by physician
2) Symptoms
- different from the normal structure/funciton
- experienced by the patient
CT
1) Computed Tomography
2) X-ray imaging that measure tissue density
- higher the atomic number the greater ability to attenuate or stop the x-rays
3) Use Hounsfield Units (HU)
- aka CT numbers
4) Provides fast and accurate method of detecting RECETN SUBARACHNOID HEMORRHAGES
- subarachnoid hemorrhage appears hyper dense (white)
- subarachnoid space and cisterns appear hypodense (black)
5) Neoplams
- areas of inflammation
- can be detected w/enhanced CT bc contrast agents leak from vessels into cellular spaces
Posterior Parietal Cortex
- function
- lesions
1) Area 5 and 7
2) strong connection to contralateral areas 5 and 7
- hemispheres communicate about motor coordination
3) Receives sensory input from the post central gyrus (1,2,3)=feedback mechanism for fine motor adjustments
- 5-> input from somatosensory and vestibular system; active when reaching for objects
- 7->input from visual cortex related to objects in space (hand eye coordination)
4) Make up 1/3 of the corticospinal tracts
- pyramidal fibers
5) Lesions:
- can’t use both hands in coordinated way to accomplish fine motor tasks
Where does the thalamus receive and send fibers to and from?
1) Premotor cortex
2) Supplementary motor cortex (M2)
3) M1
are 4 and 6
Glial Cells
1) Can’t propagate action potential
2) provide neurons w/structions support and maintain environment for neuron fxn
3) Type of Glial Cells
- Astrocytes
- oligodendrocytes
- microglia
B2-adrenergic Receptor
1) Gs coupled
2) Stimulates activity of adenylyl cyclase
ATP-> cAMP
3) endogenous ligand for this receptor=catecholamine epinephrine
Epinephrine
1) used clinically in CARDIOpulmonary resuscitation during cardiac asystole and to treat anaphylactic reactions
Propanalol
1) interferes with the binding of NE to postsynaptic
2) prescribed to manage:
- agina pectoris
- hypertension
- congestive heart failure
Norepinephrine
1) NT
2) Regulates the sympathetic division of the ANS in the peripheral nervous system
-binds to a- and b- adrenergic receptors
3) Greatest source of NE in mammalian CNS
=locus ceruleus
Demser
1) AKA a-methyltyrosine
AKA metyrosine
2) Competitive inhibitor of Tyrosine Hydroxylase
3) Pts who suffer symptoms from excess production of catecholamines from pheochromacytomas
Catecholamines
1) derived from tyrosine pathway
2) includes:
- epinephrine
- norepinephrine
- Dopamine
Reserpine
1) Plant Alkaloid
2) Earliest therapeutic agents for tx of hypertensive cardiovascular disease
3) may give Parkinson like symptoms
4) Inhibits Dopamine and Norepinephrine
5) Rarely used today to treat hypertension
ALdomet
1) A-methyldopa
2) effective antihypertensive drug during pregnancy
3) reduces the accumulation of dopamine and norepinephrine in synaptic vesicles
Guanethidine
1) Reserpine Like
2) Causes:
- excessive reduced heart rate, nasal congestion, and orthostatic hypotension
Yohimbine
1) Reserpine like
2) present in many herbal preparations and beverages
- thought to be aphrodisiac
3) promotes erectile dysfunction
Psychomotor Stimulant Drugs
1) Cocaine and Amphetamines
2) enhance motor performance, relieve fatigue, and enhance synaptic concentrations of monoamines (tyrosine pathway)
3) Cocaine
- inhibit membrane monoamine transporters
- ruduces reabsorption of monoamines out of synaptic cleft
4) AMphetamine
- inhibit MAO-A (Periphery) and MAO-B (Braine)
Tranylcypromine
1) AKA Parnate and (Phenelzine aka Nardil) 2) nonselective inhibits -block both MAO-A and MAO-B 3) treats major depressive disorders 4) Frequent side effects
Selegiline
1) AKA L-deprenyl, Eldepryl
2) selective inhibitor of MAO-B
3) Blocks mitochondrial degradation of Dopamine in CNS
4) management of Parkinson’s
Hydrocephalus
1) When CSF accumulates in ventricular spaces or around the brain
- reabsorption failure
- overproduction
- obstruction of movement
2) usually caused by:
- obstruction of CSF flow=enlargement of the ventricular space
3) Characterized by:
- Increased in CSF volume
- enlargement of one or more ventricles
- increase in CSF pressure
Hydrocephalus: Occlusion of cerebral aqueduct during development may be result of:
1) Gial scarring (Gliosis) due to infection
2) Development defects of forebrain
3) rupture of amnionic sac in utero
4) forking of aqueduct
Obstructive Hydrocephalus
1) obstruction within ventricular system or subarachnoid space
2) Common INTRAVENTRICULAR SITES:
- interventricular foramen
- cerebral aqueduct
- caudal portions of 4th ventricle
- foramen of 4th ventricle
3) Common Extraventricular sites in subarachnoid space:
- base of brain
- tentorium cerebelli
- tentorial notch
- over the convexity of hemispheres
- SSS
Aqueductal Stenosis
May be caused by:
1) tumor in midbrain
- pineoblastoma or meningioma
2) occluded by cellular debris following:
- intraventricular hemorrhage
- bacterial or fungal infections
- ependymal proliferation due to viral infections of CNS (mumps)
Major sequela (consequence)= Triventricular hydrocephalus -enlargement of 3rd and both lateral ventricles
Obstruction of foramina of Magendine and Lushka
-enlargement of all parts of ventricular system
Communicating Hydrocephalus
1) Movement of CSF through subarachnoid space into venous system is partially or totally blocked
2) Caused by:
- Agenesis (congenital absence) of arachnoid villus
- Villi partially blocked by RBC following subarachnoid hemorrhage or major CNS infection (leptomeningitis) and subsequent immune response
- overproduction of CSF in patients w/papilloma of choroid plexus
3) will have:
- High levels of proteins in CSF->500mg/dL (CNS tumors or inflammation)
- High CSF pressure
4) RESULTS:
- enlargement of all parts of ventricular system
Hydrocephalus ex Vacuo
1) Not true hydrocephalus
- but atrophy of the brain resulting in ventricles that larger due to loss of white matter
2) No increase in intracranial pressure
3) no neurological deficits other than those related to brain atrophy
Idiopathic Intracranial Hypertension
1) AKA pseudotumor cerebri
2) Most commonly seen in:
- obese women of child bearing age
- chronic renal failure patients
2) Could be related to VIT A toxicity
3) Increased in Intracranial pressure (>25 cm H2O)
- w/little evidence of pressure increase on CT or MRI scans
4) Sympotoms:
- headaches
- visual deficits (up to blindness) due to papilledema (swelling of optic disc)
Normal Pressure Hydrocephalus
1) Unclear Cause
2) CSF elevated periodically=Elevated Intracranial Pressure periodically
- may return to high-normal level
- effects of increased pressure remain
3) usually elderly patients affected
4) Sympotoms:
- diagnostic triad of urinary problems (frequency, urgency, incontience)
- impaired Gait-steps on curb
- dementia
5) Can look like a degenerate disease
- Parkinsons
- ALzheimers
Hemorrhage into Ventricles:
1) Caused by:
- hemorrhage into the brain (cerebral hemorrhage) the subsequently ruptures into ventricular space
- Rupture of an intracranial aneurysm (3rd and 4th ventricle)
- Severe head trauma
2) Blood in ventricles seen on CT
- especially acute blood
- white appearance
Tumors of Choroid Plexus
1) rare, <1% of intracranial tumors
2) most common b/w: birth- 10 y.o
3) Located:
- 4th ventricle (50-60%)
- lateral ventricles
3)2 types choroid plexus papillomas -benign -more frequent -surgical removal
choroid plexus carcinomas
- malignant
- rare
- 1) chemotherapy 2) Surgery 3) chemotherapy + radiation
CSF vs blood plasma conc.
1) CSF high conc:
- chloride
- magnesium
- sodium
2) Similar conc to Blood plasma
- creatinine
3) lower conc
- potassium
- calcium
- glucose
- proteins
- albumin
- uric acid
Normal CSF
1) clear and colorless
2) very little protein (15-45 mg/dL)
- little immunoglobulin
- 1-5 leukocytes per millilter
3) Changes from normal values useful in diagnosis
- indicative of pathological state
Lumbar puncture
1) collect a sample of CSF for analysis and two measure CSF pressure
2) Needle inserted b/w third and fourth (or fourth and fifth) lumbar vertebrae into dural sac
-spinal pressure measured
-few milliliters of fluid withdrawn
3)-sample that is removed is quickly replaced
Since average volume of CSF in adults is 120 mL/day
-rate of production is 450-500 mL/day
IF blood is CSF following lumbar Puncture; what’s next step?
1) 3 test tube test: determines where blood is from
-subarachniod hemorrhage
-traumatic tap (damage to vessel during procedure)
2) 3 successive tubes of CSF drawn
-first=blood
-2nd=little or non
-3rd=none
RESULTS In traumatic tap
3)) if all 3 tubes contain bloody CSF that is also xanthochromic
=SUBARACHNOID HEMORRHAGE
CSF cell types in: Bacterial Meningitis or brain abscesses
1) neutrophils predominate
- 1000-20,000/mL
2) Cloudy CSF
CSF cell types in: Syphilitic meningitis
1) Lymphocytes
- 200-300 cells/mL
CSF cell types in: Multiple Sclerosis
1) Lymphocytes
- less than 50 cells/mL
2) ALSO need:
- changes in the Immunoglobulin G content of CSF
- slight increase in mononuclear cells
Dura Mater
1) AKA pachymeninx
2) thick outer layer
3) does not contour brain
4) elongated fibroblasts and alot of collagen fibrils
5) Periosteal/endosteal
- outer layer
- attached to inner surface of the skull (periosteum)
- Strong attachment along suture lines and cranial base
- ends at foramen magnum of occipital bone
- Fibroblast larger and less elongated
6) Meningeal
- inner layer
- Fibroblasts flattened, elongated, nuclei smaller, and cytoplasm darker
7) Dura Border cell layer
- innermost part
- Fibroblasts flattened, sinuous processes
- no collagen present
- attached to arachnoid membrane by: cell junctions-desmosomes and gap junctions
Supratentorial Compartment vs infratentorial compartment
1) Supratentorial compartment
- superior to tentorium cerebelli
- bilateral (r and L)-seperated by Falx cerebri
2) Infratentorial compartment
- single
- inferior to tentorium cerebelli
Herniation syndromes occurs when:
1) intracranial event (hemorrhage, rapid tumor growth, traumatic brain injury) causes:
- increase in intracranial pressure-> forcing brain over edge of dural reflection
Herniation syndromes: Supratentorial compartment
1) Subfalcine or cingulate herniation
2) Central (transtentorial) herniation
3) Uncal herniation
Subfalcine Herniation
1) Supratentorial Compartment
2) AKA cingulate herniation
3) lesion in one cerebral hemisphere expands toward midline
- forces cingulate gyrus under Falx cerebri into opposite hemisphere
4) Deficits:
- oclusion of anterior cerebral artery
Central Herniation
1) Supratentorial Compartment
2) AKA transtentorial herniation
3) diencephalon is forced downward through tentorial incisure or notch
4) Neurologic emergency
- 90% of patients-serious disability or death
Uncal Herniation
1) Supratentorial Compartment
2) rapidly expanding lesion
- usually hematoma
- forces uncus over tentorium cerebelli
- damages midbrain
3) common deficits:
- decreased level of consciousness
- dilation of the pupil and loss of eye movement reflecting damage to ipsilateral oculomotor nerve
- Contralateral hemiplegia
Herniation syndromes: Infratentorial compartment
1) Upward cerebellar herniation
2) Tonsilar herniation
Upward Cerebellar Herniation
1) Infrantentorial
2) mass or pressure increases in posterior cranial fossa forces cerebellum upward through tentorial incisure
3) Damage to midbrain
Tonsilar Herniation
1) infratentorial
2) tonsils of cerebellum are forced downward into/through foramen magnum
- pressure on medulla
- damage respiratory centers
3) DEATH
Meningioma
1) Usually Single tumor
- benign
- slow growing
2) Primary intracranial tumors but not primary tumors of the brain
3) Women 30/40-60 most common
3) Arise from Arachnoid Cap cells
- arachniod cells associated with arachnoid vili
4) most found in the cranial Cavity (90%)
- spinal cord (9%)
- ectoptic meningiomas (1%)-outside CNS
5) located: in order of occurence
- parasagittal (parasagittal meningioma)
- Convexity (Convexity meningioma)-designed by lobe
- Sphenoid ridge (Sphenoid Ridge meningioma)
- Tuberculum Sellae or suprasellar
6) also found at:
- attached to falx cerebri (falcine meningioma)
- attached to tentorium cerebelli (Tentorial Meningoma)
3 types:
1) Meningotheliomatous (syncytial)
- polygon shaped w/large central nucleus
- arranged in sheets or whorls
2) Transitional
- b/w syncytial and fibrous appearance
- whorl formation
- psomma body
- small blood vessel
3) Fibroblastic
- long spindle shaped cells w/elongated nuclei
- whorl formation
- psomma body
Meningeal hemorrhage generally described as:
1) blood the strips the dura from the skull or opens the dura border cell layer
2) most common cause:
- Head injury with or without skull fracture
Extradural Hemorrhage
1) Head injury
2) Periosteal dura from skull to form EPIDURAL Space
3) Damges middle and accessory meningeal arteries
4) Blood collects to form EPIDURAL/extradural HEMATOMA
5) Increased Intracranial Pressure
5) Lesions:
-lenticular shaped
-appear short and wide
6) Neurological Deficits: in order of occurence
-headache
-confusion and disorientation
-Lethargy
-state of unresponsiveness
7) “Tak and Die”
-initially unconscious
-lucid interval (wide awake and talking)
-rapidly detoriatee
=DEATH
Subdural Hemorrhage
1) Head injury
2) bleeding into meninges b/w dura and arachnoid= Subdural Space
3) Tears Bridging vein as they pass through subarachnoid space->dural venous sinus
- Veenous blood
3) Results in Subdural Hematoma or DURAL BORDER hematoma
- splits open dural border cell layer
Subarachnoid Hemorrhage
1) usually arterial blood into subarachnoid space
2) most common cause:
-trauma
-large veins
3) most common cause of non-traumatic:
-rupture of intracranial aneurysm
-40-65 yrs old
4) 1/3 die before or soon after admission to doctor
1/3 have permanent and significant disability (cognitive and motor)
1/3 recover with minimal neurological affects
5) The occurrence of subarachnoid hemorrhage signaled:
-headache as “explosive and awful”
6) Diagnostic;
-bloody CSF via lumbar puncture
-CT exam
Meningitis
1) Baterial or viral origin
Bacterial meningitis
1) located:
-subarachnoid space
-involves leptomeninges (pia and arachnoid)
2) Causes:
-trauma
-septecemia
-metastasis from another site of infection in body
3) Classification
-acute
-subacute
-depends on how reply disease progresses
4) Most Common Causitive Agents:
-Streptococcus Pneumoniae
-Neisseria Meningitides (75%)
5) Signs and symptoms:
Acute: (days)
-elevated temp
-alternating chills and feveer
-headache
-depressed level of consciousness
-ICP
-hydrocephalus
-cranial nerve palsies
-nausea and vommiting
-neck pain
-nuchal rigidity
-petechial rash
-photosensitivity
-postive kernig and Brudzinki sign
w/ increased CSF pressure, cloudy CSF w/many WBC, Increased protein and bacteria=diagnositic
Subacute: (weeks rather than days)
- may be due to mycotic infections
- onset is slow
- headache
- fever
- irritablity
- wakefulness at night
6) Prognosis:
-excellent (90%) cure rate with early diagnosis and treatment
-recover In weeks
-can be lethal if not treated
70 Tx:
-antibiotics
Viral Meningitis
1) Commonly seen in younger patients (<25 yrs)
2) no antiviral meds available
- suportive with focus on fever pian
3) caused by range of viral agents
- enteroviruses
- mumps
- Epstein-Barr
- herpes
- Varicella-zoster (chicken pox)
- measles
- influenza
4) Pt becomes ill over a period of days and experiences:
- fever
- headaches of increasing intensity
- nuchal rigidity
- photosensitivy
- somnolence (sleepy)
- nasua and vomitting
- confusion
- altered level of consciousness
Less often: more serious sings and symptoms: -seizure -rigidity -cranial nerve palsies 5) Lumbar puncture -clear or cloudy CSF -hihg 25-500mm lymphocyte count -slightly elevated lymphocyte 6) prognosis -after 1 to 2 weeks the signs and symptoms moderate -pt recovers without permanent deficits not fatal
Fungal Meningitis
1) seen in patients w/immune deficiency such as aids
Amoebic Meningitis
1) due to infection with amoebae
- contracted from freshwater sources
Aseptic Meningitis
1) all cases of meningitis in which no bacterial infection can be demonstrated
2) usually due to viruses but can be due to bacterial infection that has already been partially treated
-disappearance of bacteria from meninges
OR
-infection in a space to the meninges (sinusitis)=caused by endocarditis
Schwannoma
1) 2x more likely in women
2) Benign Tumor
3) Acoustic Neuroma
Vitamin B12 deficiency
- name of vitamin
- fxn
- what causes
- symptoms
- signs/syndromes
1) Cobalamin
2) essential dietary nutrient found in meats
3) causes b12 deficiency:
- perniscious (unexplained) anemia (major)
- strick vegetarian diet
- inability to reabsorb vitamin
- autoimmune diseases
4) common in the US-elderly
5) Symptoms:
- serious anemia
- nerve damgae
- spinal cord degeneration
- MYELIN DAMAGE
- paresthesia
- seizuires
- developmental regression
- Dementia
6) Signs/Syndromes: Lhermitte’s sign
- AKA Babar Chair Phenomenon
- classic finding’s in MS
- electrical sensation that runs down the back and into limbs
- elicited by bending head forward
Vitamin B1 Deficiency:
- name of vitamin
- symptoms
- signs/syndromes
1) AKA beriberi
2) breakdown carbohydrates and decreases utilization of amino acids
-CNS depends on for energy
-if defective, the body will utilize ketone bodies
A) beta-hydroxybutrate (main)
-acetoacetic acid
-Acetone (Fruity Breath)
3) Symptoms
- tingling/buring sensation in extremities
- motor issues (ataxia)
- leg weakness
- pain
- vomitting
- Polyneuritis=myelin damage in PNS and CNS
4) Syndromes; Korsakoff Syndrome -chronic/irreversible -short term memory loss -alocholic dimentia -coomfabulation
Wernickee Encephalopathy
- acute/reversible
- ataxis
- opthalmoparesis
- confusion
- motor/memory loss
