Midterm 2 Flashcards
Brodmann’s Areas
Definition: Areas defined and numbered based on cytoarchitectural organization of neurons using the Nissl method of cell staining.
- Defined solely based on neuronal organization
- Correlate closely with diverse cortical functions
Univocal (modality-specific) association vortices
1) Primary sensory cortex
2) Primary motor cortex
3) Primary auditory cortex
4) Primary visual cortex
Heteromodal (higher-order) association cortices
1) Unimodal association cortex
2) Heteromodal association cortex
3) Prefrontal cortex
Primary Motor Cortex
Brodmann Area: 4 aka M1
Function: Works in association with premotor cortex, supplementary motor area, sensory and posterior parietal cortex and several subcortical brain regions to plan and execute movements.
- Precentral gyrus
- Contains somatotopic maps of contralateral body movements
- Target for cerebellum and motor thalamus projections
Lesion: Varied degrees of focal paralysis in the CONTRALATERAL side of the body or face.
Primary Sensory Cortex
Brodmann Area: 1, 2, 3
Function: Interlocked with primary motor cortex to send projections to the superior and inferior parietal lobules.
- Somatotopic map of contralateral body sensations
Lesion (General): Varied degrees of focal impairment in sensation on the CONTRALATERAL side.
Primary Sensory Cortex: Lesions
Acute (immediate stage): Loss of all sensory modalities on the contralateral side of body and/or face.
Chronic (later stage):
- Recovery of sensation of pain and temperature and crude touch sensation
- Thalamic level- sensation of pain and temp
- Sensory cortex- source, quality and intensity of pain
- Continued loss of fine aspects of tactile information on the contralateral body (arm and face)
- Loss of two-point discrimination
- Agraphesthesia
- Astereognosis
- Loss of vibration and light touch
- Continued loss of pro prince potion in contralateral body (arm and face)
- When leg is involved get positive Romberg sign (ataxia when eyes are closed)
Lesions to insulate and SII (maybe anterior cingulate)
Asymbolia for pain- Lack of motivation to avoid pain.
Agraphestesia
Inability to recognize a latter outlined on the skin.
Astereognosis
Inability to recognize form.
Organization and Pathways of the Somatosensory System
1) Dorsal root ganglion neurons respond to find touch adn pressure, pain and temp
2) Ventral spinothalamic tract receives input from pain and temp neurons and joins medial lemniscal tract
3) Dorsal column nuclei relay fine touch and pressure sensations.
4) Medial lemniscus contains axons that carry sensory information to the ventrolateral thalamus
5) Ventrolateral thalamus relays sensory information to the somatosensory cortex.
6) Primary somatosensory cortex receives somatosensory information.
- Homunculus
- Topographic map
- Disproportionate cortical representation of body parts
Temporal Lobe: Primary Auditory Cortex
Brodmann areas: 41, 42
- Transverse Gyri
- Represent acoustic frequencies and intensities of unhitched sounds to permit recognition and spatial localization
- Each receives input from both ears–> Unilateral damage does not cause deafness
- Surrounded by association auditory cortex
Lesion: Bilateral- auditory agnosia
Unilateral in dominant hemisphere- Pure word deafness
Unilateral in non-dominant hemisphere- Amusia (inability to produce or recognize musical sounds)
Temporal Lobe: Medial Temporal Lobe
- Cortical and subcortical structures of the limbic system
- Entorhinal cortex
- Hippocampal formation
- Amygdala
Lesion:
-Entorhinal and hippocampal formation = memory –> Anterograde memory impairment - Amygdala- Kluver-Bucy Syndrome
Kluver-Boucy Syndrome
Syndrome associated with lesions to the amygdala in which there is a marked decrease in the ability to express emotions.
Primary Visual Cortex
Lesions:
- Upper calcarine - lower field defect
- Macular sparing: Many blood vessels at the tip of the cortex for the center of vision so the center of vision is spared
- Blood from PCA and MCA
Prefrontal Cortex
- Contains areas that mediate higher mental functions
- Broca’s Area
Broca’s Area
Brodmann Area: 44, 45
- Lateral Sylvian fissure
- Pars triangularis and opercularis
- Connected to Wernicke’s area via accurate fasiculus
- Mostly in the left hemisphere because language lateralized to left (left-handed is three way split between left, right and both) - Language distinct from speech- speech supported by the entire motor system for vocalization
Arcuate fasiculus
Structure that connects Wernicke’s and Broca’s areas
Association Sensory Cortex
- Superior and inferior parietal lobules
- Connects Wernicke’s and Broca’s areas
Lesion: - Dominant hemisphere
- Inferior parietal lobule
- Angular gyrus: Alexia and agraphia (inability to read written language and inability to write language)
- Supramarginal gyrus: Conduction aphasia
- Superior parietal lobule- Optic ataxia in contralateral hand
- Can’t use the visual system to guide motor movements so reaching for anything is like reaching into the dark - Non-dominant hemisphere
- Inferior parietal lobule- Anosagnosia (unaware of their condition)
- Left visual field neglect (can’t follow previously known and automated route, not hit obstacles on left side, can’t learn new route) - Superior parietal lobule- Optic ataxia
- Inferior parietal lobule- Anosagnosia (unaware of their condition)
Object Agnosia
- Bilateral inferolateral parts of occipital lobes
- Patient fails to name or indicate the use of a seen object
- Vision is intact because patient can see an object but can’t tell what it is
- If object is touched or smelled or makes a sound then it can be recognized
Achromatopsia
Failure to recognize color.
- Inferior occipital cortices
- Sparing calcarine cortex
- Contralateral
Prosopagnosia
Inability to recognize faces but able to see the face.
- Bilateral occipitotemporal
Anton’s Syndrome
Denial of blindness
- Bilateral occipital cortices from calcarine and extending superiorly to parietal cortex.
Anatomical and Functional Asymmetry
- Slope of lateral (sylvian) fissure differs
- Wernicke’s area mostly left hemisphere
- More auditory cortex in the left
- Left more verbal and right is more non-verbal
- Left temporal lobectomy: Low verbal recall
- Right temporal lobectomy: Low non-verbal recall (performance IQ too, but may be unrelated)
Commissurotomy
Split brain
- Put object in left hand, patient cannot name object but if you put the same object in the right hand patient can name it
The Wada Test
Function: Determines which side language is lateralized on before surgery
- Sodium amobarbital injected into carotid artery where it anesthetizes the hemisphere on the side of injection
- On left side patient shouldn’t be able to speak if speech is lateralized there
Damage to right parietal cortex
Anosognosia
- Denial of illness or failure to recognize
- Apathy/placidity
- Paralyzed on left side of body but say they could move it, or reason that they don’t need that side so it’s okay
- After a while they will come to accept that they’ve had a stroke but still not full acceptance like a normal patient - Left-sided damage leads to aphasia and patients are cognizant of their deficit and often feel depressed
Clinical Case: What functional sensory and motor systems are affected in this patient?
1) Upper Motor Lesion: Inability to grasp, dragging left leg and Babinski’s sign
- Corticospinal tract: Arm and leg involved, above C4
- Facial nerve: Above level of facial nuclei because of lower face paralysis
2) Somatosensory cortex: Intact primary modalities (pain and temperature) but loss of cortical modalities (proprioception, graphesthesia, two-point discrimination, localization of light touch) on left side –> Only occurs when the thalamus is spared
(In other words: intact elementary sensation and impaired discriminative sensation suggest a lesion of right hemisphere rostrum to the right thalamus)
Clinical Case: At what level of the CNS are they affected?
Cortex
(Evidence: Somatosensory cortex damage- primary modalities in tact like pain and temperature/touch, but cortical modalities like proprioception and graphesthesia and two-point discrimination aren’t in good shape)
(Evidence: Right-sided lesion between frontal eye fields and midbrain would affect corticospinal tract which explains left-sided weakness, and cause left gaze paresis because damage to these circuits causes contralateral eye deviations and the eye deviates to the left)
(Evidence: Supranuclear disorder of gaze- oculovestibular functions intact (doll’s head) but can’t move voluntary –> Lesion must be above the level of Rochelle, oculomoter and abducens nuclei and nerves and the. Medial longitudinal fasiculus is intact)
Clinical Case: Why is the patient’s gaze direct to the right?
Lesions in the right side of the brain cause left gaze palsy.
Clinical Case: Why does the patient have a left gaze palsy?
The patient cannot move their eyes to the left because of frontal eye field lesions.
- Stimulation causes ipsilateral deviation and destructive lesions cause the eyes to deviate contra-laterally
- Lesion above the lower midbrain of pathways from the right frontal eye fields will prevent the patient from looking to the contralateral side - Frontopontine tract from motor cortex to PPRF on contralateral side, right near motor facial representation
- Lesions cause eyes to deviate to the side of lesion
- Lesion above lower midbrain of patient in pathways from FEF will prevent patient from being able to make left gaze
Clinical Case: How would you test this patient’s vestibule-ocular movements?
You would use doll’s head movements- Changing vestibular system causes the eyes to move to maintain fixation as the head moves.
Clinical Case: Discuss the patient’s visual sensory deficit and provide the appropriate neurological/opthamological name for it.
Name: A left homonymous hemianopsia
- Follows right-sided lesions of the retrochiasmal afferent visual system which includes the optic tract, lateral geniculate nucleus, optic radiations and occipital cortex.
- Some of these regions past the chiasm cause foveal sparing, so it must be optic radiations
- Optic radiations are just near the motor and sensory cortex and frontal eye fields, so extend the lesion to these areas and anatomical diagnosis is complete
Clinical Case: Why is the abrupt onset of symptoms significant for this patient?
Symptoms that quickly appear usually indicate a vascular incident (stroke), or electrical incident. The patient likely does not have a tumor since those grow gradually and progressively affect behavior and generate deficits.
- Vascular has negative symptoms while electrical has positive --> This case is all negative symptoms so it's vascular and from occlusion because no headache - Middle cerebral artery stroke because that supplies most of motor and sensory cortices as well as frontal eyes fields which is all the stuff affected in this case - Supplies optic radiations as well- responsible for gaze problems - Patient's diabetes mellitus and hypertension increase risk for antherosclerotic disease, making ischemic stroke even more likely
Clinical Case: Cause of stroke
Emobolus from left atrium to right middle cerebral artery.
Posterior Cerebral Artery supplies….
Visual cortex, upper brain stem and inferior temporal lobe
Anterior cerebral artery supplies….
Frontal and medial cerebrum - strokes cause lower extremity sensory and motor loss.
Middle cerebral artery supplies….
Lateral aspects of the cerebrum including most of the sensory-motor cortices and frontal eye fields. Also supplies underlying white matter like the optic radiations
- Stroke in this area creates pattern of symptoms described in this case
Five elements of a neurological exam
1) Cranial nerves
2) Motor system
3) Sensory system
4) Coordination/balance/gait
5) Mental status
Which cranial nerves provide taste?
Facial, gossopharyngeal and vagus
7, 9 and 10
Clinical Tests: Cranial Nerve I (Olfactory)
Testing: Smell
- Damage can lead to traumatic anosmia
- A special kit has numerous packets that store various smells. The examiner scratches one packet at a time and asks the patient to identify the smell.
- This is done by closing one nostril and testing the other.
Clinical Tests: Cranial Nerve II (Optic Nerve)
Testing: Vision
- Visual acuity (20/30 means vision at a distance of 20 feet healthy vision sees at 30 feet)
- Papilledema: Optic disk is enlarged so there’s probably high intracranial pressure
- Diabetes: A lot of blood vessels harden so there’s no good blood flow to the eyes
- Testing visual fields and defects
- Confrontation method: Done with fingers of doctor and is less precise
- Perimetry: Done with a computer and is more precise.
Clinical Tests: Cranial Nerve III (Oculomotor)
Testing: Eyeball movement
Looking for…
- Ipsilateral lateral strabismus – eye is down and out
- Ipsilateral ptosis (if the eyelid is retracted have diplopia)
- Ipsilateral mydriasis – dilated pupil
- Loss of direct and consensual pupillary light reflexes in the ipsilateral eye
Clinical Tests: Cranial Nerve IV (Trochlear Nerve)
Testing: Eyeball movement
Condition….
- Trochlear nerve palsy: Patient complains of diplopia when walking down the stairs
Looking for…
- Patient tilts head away from the side of the lesion (to compensate for the alignment of both eyes and help relief of diplopia
- Ipsilateral eye points up and out
Clinical Tests: Cranial Nerve VI (Abducens)
Testing: Eyeball movement
Symptoms: Medial strabismus
- Medial rectus muscle is unopposed and pulling the eyeball medically
Clinical Tests: CN V (Trigeminal)
Testing: Face sensation
Tests….
- Pin pricks
- Vibrations
- Light touch on various areas of the face
- Moving jaws and asking for direction of movement (proprioceptive)
- Ask the patient to bite and see if their jaw deviates to the side of a lesion
Clinical Tests: Cranial Nerve VII (Facial)
Testing: Face movement
Peripheral Facial Palsy: Droop of lower and upper face.
- Lesion is lower
Central Facial Palsy: Droop of lower face
- Lesion is upper
Clinical Tests: Cranial Nerve VIII (Vestibulocochlear)
Testing: Hearing and equilibrium
Tests….
- Listening
- Balance
Clinical Tests: Cranial Nerves IX, X, XI, XII (Glossopharyngeal, vagus, accessory and hypoglossal)
Testing: Pharynx movement/sensation, tongue movement and head and shoulder muscle strength
Gossopharyngeal and Vagus:
- Gag reflex
- Hoarse voice
- Difficulty swallowing
- Look for symmetrical soft palate movement
Hypoglossal
- Stick tongue out and deviates to side of lesion
Accessory
- Place hands on patient’s shoulders or check and have them shrug shoulders or push face against resistance
Corticospinal Tract (Basic Review)
- About 90% of corticospinal tract fibers cross
- Carry motor system messages from motor cortex to lower motor neurons
Clinical Tests: Motor System
- Grading muscle strength 0 no movement 1 muscle twitch, no movement of limb 2 muscle contracts but no movement against gravity 3 able to provide minimal resistance 4 above to provide moderate resistance 5 normal strength
- Grading muscle tone: Normal, decreased (flaccid) or increased (rigid, spastic, cogwheeling)
- Decorticate Thumb: Thumb is tucked under flexed fingers in fisted position, can’t hold a pencil properly
- Abnormal reflexes
- Spinal reflex arc (patellar reflex)
- Babinski sign
Clinical Tests: Sensory System
Testing: Sensation
- Check pain and temp with pin prick
- Check vibration/discriminative touch with two point test
- Check proprioception with Romberg sign
Romberg Sign
Patient loses their balance once their eyes are closed, but is able to maintain it with no problems when their eyes are open
Clinical Tests: Coordination/balance/gait
Structures involved: Cerebellum and basal ganglia
Cerebellum: Feedback control, midline structures (vermis) associated with gait and balance disorders
- Intention tremor
- Finger to nose and hell to shin testing
- Simple and complex finger movements
- Three step motor movements
- Heel to shoe walking
- Romberg test
Basal Ganglia
- Parkinson’s (degeneration of substantia nigra)
- Stage 1: Unilateral involvement, blank faces, tremor and patient leans to unaffected side
- Might notice difficulty grabbing cup or buttoning shirt
- Stage 2: Pronounced gait disturbances and moderate generalized disability- postural instability with tendency to fall
- Stage 3: Bilateral involvement with postural changes- slow shuffling gait with decreased excursion of legs - Huntington’s Disease (loss of caudate)
- Ventricles now have more boxy shape because no caudate– “box caring” of the ventricles
Nigrostriatal Pathway
Dopamine goes from the substantia nigra (midbrain) to the caudate/putamen (striatum)
Symptoms of Parkinson’s
1) Bradykinesia
2) Retropulsion
3) Masked faces
4) Stoppped posture
5) Resting tremor
6) Led Pipe Rigidity
Symptoms of Huntington’s
1) Quick jerks; rapid movements
2) Tone = loose
3) Towards the end patient has trouble swallowing due to twitching
Symptoms of cerebellar problems
1) Broad based gate
2) Can’t tandem
3) Speech slurred
4) Rapid alternating movements off
5) Intention tremor
6) Limb control off
Requirements of a coma
1) Damage to reticular activating system
- Largescale damage to the thalamus can give you these issues
2) Both hemispheres impaired
*Generally occur with dorsal damage to the brainstem (back)
Evaluation of a coma
1) Cranial nerves- if any are abnormal consider brainstem injury
2) Pupil reflexes- Midbrain problems
3) Breathing patterns- All brainstem
4) Posturing
- Decorticate - midbrain
- Decerebrate - pons
Criteria for brain dead
Definition: No neurological activity above the level of the medulla
1) Pupils fixed and dilated
2) All facial muscles not responding
3) No breathing
4) No brainstem evoked potential
Five elements of the Mental Status Exam
1) Attention
2) Language
3) Memory
4) Visuospatial
5) Executive Function
Mental Status Exam: Attention
Anatomy: Focal (cortical or subcortical), diffuse (metabolic, toxic, infectious)
- Diffuse could be drunk, metabolic disease
- Focal could be neglect
Exam:
- Observe patient
- Orientation (person, place, time)
Differences between a coma and brain dead
Coma: Some brain activity, reflexes and EEG, but not conscious
Braindead: No brain activity and the brain completely isn’t functioning
Mental Status Exam: Memory
Anatomy: Medial temporal lobes (home of the hippocampus), thalamus, basal forebrain
Exam:
- Remember 3 words for 5 minutes
- Remember 3 shapes for 5 minutes
- Past public and personal events
- Factual knowledge
Mental Status Exam: Language
Anatomy: Left hemisphere
Exam:
- Fluency
- Naming
- Repetition
- Comprehension
- Reading
- Writing
- Broca’s aphasia
- Non-fluent
- Difficulty naming
- Good comprehension - Wernicke’s aphasia
- Fluent
- Incomprehensible
- No comprehension
- Lack of awareness
Mental Status Exam: Visuospatial/Perceptual
Anatomy: Right hemisphere
Exam:
- *Copy of geometric designs
- Judgement of line orientation
- Object/face/color recognition
- *Line cancellation
- Can neglect both the left side of the line thus cutting too far right, or the entire left side of lines not cutting any from the left - Graphesthesisa (something traced in hand)
- Astereognosis (object in hand)
*Looking for left neglect because of lesion in right parietal cortex
Mental Status: Executive Function
Anatomy: Frontal lobes
Exam:
- Affect
- Verbal fluency
- Sequential motor ability
- Delayed alternation
- Snout (pucker lips out when tap above the lip), suck, grasp (grasp finger when you put it in palm), rooting (Turn toward where you’re being stroked on the side of the cheek)
Stroke
Definition: An injury to the brain caused by the interruption of blood flow to a focal area of the brain or by bleeding into or around the brain.
- Cause the student onset of focal neurological deficit or headache which lasts for at least 24 hours or leads to death
Transient Ischemic Attack (TIA)
Definition: Sudden onset of a focal neurological deficit or presumed vascular origin which lasts less than 24 hours (15-20 minutes).
- About 10% of strokes are preceded by a TIA
- Highest risk for stroke is 1 week after TIA
Types of stroke
1) Ischemic (83%)
2) Hemorrhagic (17%)
Ischemic Stroke
Definition: Obstruction of a blood vessel supplying the brain by a blood clot deprives the brain of essential nutrients and if blood flow is not restored quickly leads to irreversible damage to the area of the brain supplied by the blood vessel. Four subtypes: 1) Antherothrombotic 2) Cardioembolic 3) Lacunar stroke 4) Other causes
Antherothrombotic Ischemic Stroke
Definition: Antherosclerotic plaque ruptures causing platelet aggregation and thrombus formation can develop directly on the plaque in the intracranial vessels.
- Most common stroke type in those over 50
- Risk factors: Hypertension, smoking, diabetes, elevated cholesterol
- Use antiplatelet therapy to prevent risk of another stroke
Cardioembolic Ischemic Stroke
Definition: A thrombus arises in the left atrium, left ventricle or mitral or aortic valve and then travels, lodging in branch points in the cerebral blood vessels.
- Multiple strokes in different arterial territories suggest this subtype
- Second most common type of ischemic stroke
- Treatment: Anticoagulation therapy (warafarin) to prevent recurrent stroke
Lacunar Ischemic Stroke
Definition: Small blood vessels are affected by thickening of the vessel wall and cause occlusion.
- Risks: Hypertension, diabetes
- 15% of ischemic strokes
- With multiple attacks can lead to multi-infarct dementia
Other causes of ischemic stroke
Possible causes:
- Blood disorders (hypercoaguable state or hemoglobinopathy)
- Dissection of the blood vessel wall due to illicit drugs
- Autoimmune process (vasculitis)
- Obstruction of the veins
Ischemic Penumbra
Definition: The area around the central core of tissue that is damaged that has only reduced metabolic activity and is still viable if perfusion is restored.
- Over time the penumbra shrinks and central core enlarges
- Treatment with thrombolytic agents such as TPA must occur within 3 hours to save any tissue
Cellular mechanisms of stroke
Initial: Decreased energy production with failure of ionic pumps and mitochondrial injury
- Leads to production of free radicals and activation of leukocytes
After: Release of excitatory neurotransmitters (glutamate) which cause further injury with influx of sodium, calcium and chloride ions
Final: Release proteases which break down the cytoskeleton and DNA
-Clinical trials look for drugs which block these secondary effects (glutamate receptor blockers, inhibit inflammatory response or block production of free radicals) but to date no effective “neuroprotective agent” has been found which works in humans. *Active area of stroke research
Hemorrhagic Stroke
Definition: Bleeding into the brain substance or around the brain. Types of hemorrhagic stroke 1) Intracerebral hemorrhage 2) Subarachnoid hemorrhage 3) Extradural (epidural) hemorrhage 4) Subdural hemorrhage
Intracerebral Hemorrhage
Definition: Stroke in which small penetrating arteries rupture with bleeding
- Most common cause: Hypertension
- Other causes: rupture of arteriovenous malformations (Connection between arteries and veins not strong so they “blow up”), bleeding into a brain tumor, coagulation defects, or vasculitis - Symptoms: Headache, nausea or vomiting and focal neurological deficit
- Need CT scan ASAP to differentiate from ischemic
Subarachnoid Hemorrhage
Definition: Bleeding into the subarachnoid space
- Cerebrospinal fluid contains blood because it circulates from here
- CSF looks yellow because of blood breakdown components for 3-10 days following hemorrhage - Symptoms
- Worst headache of a patient’s life
- Loss of consciousness
- Nausea and vomiting
- Neck stiffness
- Focal neurological findings - Most common cause: Cerebral aneurysm
- After stroke risk of vasospasm of vessels in circle of willis which causes ischemic stroke and is usually fatal – medications can prevent this
- Kernig’s Sign: Resistance to full extension of the leg
- Can be fixed with surgical clip- most popular
Extradural Hemorrhage
Definition: Bleeding between the skull and dura mater
- Damage to branches of middle meninges like artery which occur following even minor head trauma
- Bleeding extends into Extradural space
- Form slowly because of tight attachment of dura to skull- clinical signs may not occur for hours, even days after injury
Subdural Hemorrhage
Definition: Bleeding between dura mater and arachnoid mater
- Superficial cerebral veins pierce the arachnoid and bridge the subdural space to enter the superior Sagittarius and transverse sinuses
- Bridging veins are torn in head trauma
Prevalence of each mechanism of stroke
Thrombotic ischemic (60%) Embolic ischemic (20%) Hemorrhagic (20%)
Risk Factors for Stroke
1) Hypertension
2) Cigarette smoking
3) Diabetes
4) Hypercholesterolemia
5) Overweight/lack of exercise
Carotid Endarterectomy
Surgery to remove plaque buildup in the carotid artery to prevent occlusion.
Middle Cerebral Artery Stroke
- Will be seen on scans on the sides of the brain
- Complication: Edema
- Brain has nowhere to expand so it can cause herniation
Posterior Cerebral Artery Stroke
- Bilateral lesions in posterior cortex in fusiform gyrus causes prosopagnosia
Types of aneurysms
1) Berry- Round
- Most commonly found between branches of the circle of willis
2) Fusiform- Vein looks crumpled and not smooth
Causes of dementia
1) Neurodegenerative disorders
- Alzheimer’s disease
- Pick’s disease
2) Vascular (multi-infarct) dementia
3) Reversible causes
Alzheimer’s Disease deficits
Cognitive
- Profound memory loss
- Language (atomic, empty, circumlocutory)
Behavioral
- No significant early changes in personality
- Unawareness or denial of illness
- Psychosis
Sensory and Motor
- None
Age of Onset: 70s-80sPathology of Alzheimer’s
- Neurofibrillary tangles (Tau protein)
- Start in the medial temporal lobe (hippocampus)- explains memory issues
- Primary cortices mostly spared - Amyloid plaques (Beta amyloid)
- Almost no sparing of anything
Treatments for Alzheimer’s Disease
1) Cholinergic replacement
- Cholinergic cells in the nucleus basalus are degenerated so you replace acetylcholine that is no longer being produced by cholinergic cells
- Not as effective in real life as in lab studies
2) Anti-amyloid agents
- New drugs that try this don’t really help
Genes linked to Alzheimer’s Disease
1) Amyloid Precursor Protein (APP)
- Familial early onset of AD
2) Presenilin (PS) 1 and 2
- Familial early onset of AD
3) Down’s Trisomy 21
4) ApoE4
- Increased risk of late onset of AD
5) Tau (MTAP) Mutations
- Fronto temporal dementia, not AD
Factors that can help delay the onset of Alzheimer’s Disease
1) Estrogen replacement
2) Education
3) NSAIDs (Non-steroidal anti-inflammatory drugs)
Pick’s Disease: Deficits
- Frontal dementia– starts in frontal lobes
- Cognitive deficits
- Profound executive dysfunction
- Good memory, language, visuospatial skills preserved early on - Behavioral deficits
- Early prominent personality changes
- Poor judgment, insight, disinhibited, labeled, euphoric, socially inappropriate, sexual indiscretions - Frontal release signs on neurological exam but no sensory or motor deficits (suck, rooting, grasping, etc.)
- Age of onset: 50s - 60s
Pathology of Pick’s Disease
- Pick’s bodies
- Spherical aggregations in brain matter
Differences between Pick’s and Alzheimer’s Disease
- Alzheimer’s highly concentrated in medial temporal lobes
- Pick’s highly concentrated in frontal lobes
Vascular (Multi-infarct) Dementia
- Not a linear progression
- Results from lots of TIAs
- Every time you have one a new function is lost and it’s instantly gone and nothing happens until the next one
Reversible Causes of Dementia
- Intoxication
- Delerium - Metabolic abnormalities
- Renal failure
- Substrate deficiencies
- Hypothyroidism - Depression (pseudodementia)
- Infectious agents
- Neurosyphilis/fungal meningitis/HIV
Work up of dementia
- Careful history
- Complete mental status and neurological exam
- Blood studies: CBC, electrolytes, LFTs, B12, folate levels, thyroid function tests, VDRL, FTA, HIV
- Lumbar puncture
- EEG
- MRI
- PET
