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276 Cards in this Set

  • Front
  • Back
What arteries supply the anterior and posterior circulation?
Internal carotid arteries

Vertebral and basilar arteries
What is caused by an ACA, MCA, and PCA lesion?
ACA Lesion – CL leg and foot

MCA Lesion – CL, hand, arm, and face - Language maybe , Vision maybe (ML)

PCA Lesion – CL visual disturbance
Lesion of what artery causes locked in syndrome?
basilar artery
Lesion of what artery causes lateral medullary syndrome?
Lateral medullary syndrome
Lesion of what artery causes damage to both the corticospinal and DCML?
ASA (think medulla)
What sends blood to internal capsule?
MCA
What can result in ambulatory spastic hemiparesis with hemihypoesthesia ?
Capsular or Lacunar Infarct
What disease causes Thalamus & BG lit up on MRI?
CJD
What disease is associated with enlarged ventricles?
Huntington's
From superior medial to inferior lateral, what is the body parts affected?
HAL
Head
Arm
Legs
What are the 3 dural septa?
Falx cerebri- fold that lines the longitudinal fissure
Falx cerebelli- runs along the vermis of the cerebellum
Tentorium cerebelli- horizontal dural fold extends into the
transverse fissure
VPL damage results in what type of deficits?
loss of CL sensation
What fibers go through the internal capsule, cerebral peduncles, and pontine base?
CST
What are the 2 types and 4 subtypes of stroke? What are the majority?
Main type: Ischemic (80%)
Subtypes: Thrombotic (53%) and Embolic (31%)

Main Type: Primary Hemorrhagic (20% of Strokes)
Subtypes: Intracerebral Hemorrhage 10%, Subarachnoid Hemorrhage 6%
ACA Damage and Clinical Symptoms?
Paralysis and sensory impairment of contralateral leg and foot
Focal Ischemia- Left Side (Dominant) MCA?
Right face, hand and arm weakness, somatosensory deficits and language problems
Focal Ischemia- Left Side (Dominant) MCA
Right face, hand and arm weakness, somatosensory deficits and language problems
What are Broca's and Wernicke's lesions? What lesions will cause Broca's and Wenicke's aphasia?
Broca’s (expressive aphasia-related to speech production)
Wernicke’s aphasia (receptive aphasia-related to interpretation of speech)

left MCA, superior
left MCA, inferior
A lesion in which region would cause the following symptoms?

Difficulty speaking
Slow, labored speech
No Prepositions and conjunctions
Dysarthria
Good comprehension
Aware of problem
agraphia:
Broca's area
A lesion in what area will cause the following symptoms?

deficit of auditory comprehension
Cannot monitor conversation
Unaware of making mistakes
Verbal paraphrasia
Phonemic paraphrasia
jargon aphasia
Wernicke's
Posterior Association Area (parietal portion): lesion to dominant (usually LEFT) hemisphere
"Gerstmann's syndrome,"
finger agnosia (inability to recognize different fingers)
agraphia (inability to write)
alexia (inability to read)
agnosia (inability to synthesize, correlate or recognize multisensory perceptions)
dyscalculia (decreased ability to calculate or use numbers)
left-right confusion
Posterior Association Area (parietal portion): lesion to nondominant (Usually Right) hemisphere
hemineglect, contralateral neglect, extinction
constructional apraxia (disturbances in drawing)
disturbances in the awareness of the body image
anosognosia: denial (ie lack of awareness) that there is anything wrong
What is unique about a parietal lobe lesion?
The brain can recover (see painting)
What's the disease associated with hemineglect?
Focal Ischemia- Right Side (non-dominant) MCA
Posterior Association Area (parietal portion): lesion to nondominant (Usually Right) hemisphere
hemineglect, contralateral neglect, extinction
constructional apraxia (disturbances in drawing)
disturbances in the awareness of the body image
anosognosia: denial (ie lack of awareness) that there is anything wrong
MCA Damage and Potential Visual System Problems, match lesion to symptoms:

1. frontal lobes
2. radiation in temporal (Meyer's loop)
3. optic radiation in parietal and temporal lobes
4. upper portion of internal capsule and corona radiata
1. damage to conjugate eye movement to contralateral eye
2. quadrantanopia
3. hemianopia
4. capsular (motor) hemiplegia
What infarcts cause Contralateral homonymous hemianopia?
Focal Ischemia PCA Territory
What supplies STT in medulla?
PICA and vertebrals
What supplies DCML and CST in medulla?
ASA
What supplies pons?
basilar/ SCA
Damage in the medulla causes contralateral or ipsilateral in the tracts?
contralateral to all
What controls this:

Controls ipsilateral tongue (CN XII)
Speech and swallowing (CN IX, X nucleus ambiguus) (test with gag reflex)
Salivation (CN IX inferior salivatory nucleus)
Pain, temp crude touch from ipsilateral face and dura (CN V, VII, IX,X)
Vestibular and auditory inputs (CN VIII)
Taste (nucleus of solitary tract CN VII, IX, X)
Visceral sensory input (blood O2, MAP, CN X)
Sympathetics descend from hypothalamus toward preganglionic cell bodies ipsilateral spinal cord
medulla
Medial Medullary Syndrome
DCML and CST contralateral, ipsilateral XII tongue. Deviates toward weak side.
Hypoglossal lesion
tongue tilts to affected side
Lateral Medullary Syndrome- Wallenburg syndrome

What causes it?
Symptoms?
Occlusion of branches of the PICA or Vertebral

STT contralateral
ipsilateral lack of eye sympathetics (Horner's Syndrome)
ipsilateral loss of facial STT
Nucleus Ambiguus (IX and X) dysphagia
Vestibular loss- vertigo, nystagmus
cerebellum- limb ataxia

trigeminal damage (ipsilateral)

nucleus ambiguus (IX and X motor nucleus)
What does an AICA hit affect? Where?
rostral medulla
hearing
PICA or Vertebral HIT
can affect ________, but not ______.
balance
hearing
Hits in the Pons will be contralateral or ipsilateral to the tracts?
CL to all tracts
What CN are in pons?
Eye Abduction (CN VI)
Mastication (CNV)
Facial Expression and eye blink (CN VII facial motor nucleus),
Tearing and salivation (CN VII superior salivatory nucleus)
Fine touch, vibration, proprioception from face (and dura) CN V trigeminal nucleus
Vestibular input (CN VIII)
What is caused by basilar artery occlusion (pons)?
facial- paralyzed ipsilateral face

abducens- lack of lateral gaze in ipsilateral eye and ipsilateral conjugate gaze

Main trigeminal nucleus, if lesion extends rostrally- fine touch and sensation ipsilateral

Medial lemniscus, if lesion extends anteriorly- Loss fine touch, vibration, and proprioception from CL body

Spinothalamic tract, if lesion extends anteriorly &laterally- Loss pain and temp from CL face & body

Descending spinal trigeminal tract, if lesion extends sufficiently laterally- Loss pain temp from
ipsilateral face
Acoustic Neuroma ( vestibular Schwannoma)
Vestibulocochlear nerve
Vestibular division- vertigo
Cochlear division- hearing
Facial nerve- face weakness and taste
Where are the tracts in the midbrain? Damage would be CL or IL?
DCML- fine touch, proprioception, and vibration from contralateral body
STT –pain and temperature from contralateral body (contiguous with the ML)
CST –descending contralateral motor control in crus cerebri/peduncles
What important structures are in the midbrain?
Periaqueductal gray – component of the intrinsic analgesia system
Substantia nigra (source of dopamine)
Red nucleus (rubrospinal tract)
Tectum (colliculi contribute to saccadic eye movements, pupillary light reflex, and reflexive orientation to auditory stimuli)
What causes locked-in syndrome? Where is the hit? What is spared?
bilateral ventral pontine infarcts, hemorrhage, tumor, encephalitis, MS, central pontine myelinolysis

hit: Corticospinal
Lower corticobulbar
Abducens

spared: Medial lemniscus
Spinothalamic
Spinal trigeminal
Facial motor
What is Central Pontine Myelinolysis?
Noninflammatory, demyelinating condition associated with rapid correction of hyponatremia (rapid fluctuations in electrolyte status). Originally described in alcoholics and malnourished persons, and now associated with transplant patients
What would CN damage in the midbrain cause?
Eye movement control (CN III and IV)
Eye lid retraction (CNIII)
Pupil constriction and lens thickening (Edinger-Westphal & PSIII)
What's involved in Weber's syndrome?
Artery? Lesion site? Symptoms?
PCA branches

Site: Cerebral peduncles
Corticospinal tracts and descending cortical control of brainstem UMN
Symptoms: Hemiparaesis, spastic hemiparalysis, babinski, Loss superficial reflexes in contralateral body
Hemiparasis, or hemiparalysis in contralateral lower face, tongue weakness without atrophy deviation away from lesion

Site: Oculomotor nerve
Symptoms: Paralysis of ipsilateral eye with ptosis, mydriasis (pupil dilation), lateral strabismus –eye rolls down and out
Where are the possible lesion sites with a pineal tumor? What are the corresponding signs and symptoms? What is the syndrome?
Site: Vertical gaze center
Lesion: Loss vertical gaze, eyes deviate downward

Site: Vergence center
Lesion: Nystagmous on eye convergence

Site: Posterior commissure
and tectum
Lesion: Loss pupillary light response, possibly with accomidation intact

Parinaud Syndrome
What is Nystagmous on eye convergence and what causes it?
involuntary movement on eye convergence

midbrain-Pineal tumor, tectal infarct
Epidural hematoma?
Blood source:
Shape:
Blood source: Middle Meningeal Artery
Shape: Lens shaped
Subdural hematoma?
Blood source:
Shape:
Blood source: bridging veins
Shape: Crescent-Shaped
Subarachanoid hematoma?
Blood source:
Shape:
Where does blood travel?
What phrase do they say?
Blood source: from arteries within pial membrane
Shape: texaco star
CSF
"worst headache of my life”
Who has increased risk of tear to the bridging veins?
Alcoholics & elderly
What is the Monro-Kellie Doctrine?
As the volume of one component increases the volumes of the others compensate to maintain ICP (0-15 mm Hg) and to prevent neurological changes

As an intracranial mass increases in size
CSF is displaced into the spinal canal
Blood volume is reduced in the brain
Displacement of brain tissue = herniation
how does cranial perfusion pressure, mean arterial pressure, and intercranial pressure relate to one another? What are normal values?
CPP = MAP -ICP

CPP Cerebral Perfusion Pressure = 80-100 mm Hg

MAP (mean arterial Pressure) = 50 – 150 mm Hg
MAP = systolic + (2x Diastolic)/ 3

ICP (intracranial Pressure) = 0-15 mm Hg
When a fundoscope indicates high pressure, what do you not do? What do you do?
do not lumbar puncture (brain will herniate)

monitor ICP and relieve pressure (burr hole)
What is the optic disk?
blind spot where arteries and veins emerge
What does papilledema look like?
What is it caused by?
Blurred disc margins
Capillary & venous dilations
Striated optic nerve fibers
Retinal hemorrhages

high ICP
What are are two major classes of herniation?
The supratentorial (occurs above the tentorial notch) Uncal, transtentorial (central), cingulate, and Transcalvarial

The infratentorial (occurs below the tentorial notch) upward transtentorial and tonsillar.
Where does CSF travel (production to finish)?
choroid plexus (red capillary tufts in pictures) --> the ventricles --> the lateral (foramina of Luschka) and median (foramina of megendie) apertures in the walls of the 4th ventricle --> subarachnoid space --> arachnoid granulations --> dural sinus (venous circulation)
How can you tell the difference between SAH and traumatic tap?
The presence of erythrocytes can indicate
subarachnoid bleeding (if RBC + then spin serial vials of CSF, if clear = traumatic spinal tap, if xanthrochromatic = SAH )
What distinguishes bacterial meningitis CSF?
purulent CSF and elevated protein levels
Where do you put the needle for lumbar puncture?
between L3 and L4
What causes higher opening pressure?
all types of meningitis and SAH (from the bleeding)
What causes higher PMNs and what causes higher leukocytes in CSF?
PMNs- bacterial
leukocytes- TB and viral meningitis
What causes normal to higher protein levels?
viral meningitis
What 2 things cause lower glucose in CSF?
bacterial and tuberculous meningitits
What are the generalized symptoms of meningitis?
Fever, headache, stiff neck & or change in mental status
What are the cell types of the CNS?
oligodendrocytes- make myelin
astrocytes: Form support for CNS (lactate)
help form Blood Brain Barrier
Secrete neurotrophic factors
take up K+, neurotransmitters
Remove EAATs (excitatory amino acinds-GLUT

microglia- scavengers (macrophages)

ependymal cells- Form barriers
between compartments
What are the cell types of the PNS?
schwann cells- make myelin and secrete neurotrophic factors

satellite cells- support cell bodies
In the CST, what layer does neuron 1 start in? Where does LMN (neuron 2) start? Where is crossover?
Neuron 1 pyramidal cell cell body in layer V of the cortex

Neuron 2 cell body in anterior horn spinal cord = LMN (innervates muscle

caudal medulla
In the midbrain, pons and medulla, where is motor and where is sensory?
All motor is anterior
& sensory is posterior
How does the CST cross in the caudal medulla?
Across and up the pyramidal decussation
What are the medullary pyramids?
The medullary pyramids are two parallel ridges that run the length of the anterior medulla they have CST axons within
What is in the precentral gyrus?
primary motor cortex
In the cortex, what are the major input and output layers?
IV = major input layer; V = major output layer
What cranial nerve is carried in the colliculi?
CN IV
What does a PCA hit cause?
Contralateral paralysis, contralateral tongue hit and visual problems
What causes the normally uncommon CN XII lesion? What are the 2 types and what symptoms do each cause
congenital abnormalities
(foramen magnum)

UMNL (upper motor neuron lesion)
Supranuclear (eg cortex)
Contralateral atrophy and deviation

LMNL (Lower motor neuron lesion) Peripheral to brain stem Ipsilateral atrophy and deviation
What is normally seen in a LMN CN XII lesion?
LMNL (Lower motor neuron lesion) Peripheral to brain stem Ipsilateral atrophy and deviation
The atrophy seen on the left side of this individual’s tongue would be due to damage to the left hypoglossal nerve
What kind of neurons do LMNs use? What is their other name?
Use large, fast, myelinated axons
ie type A, subtype alpha

motor neurons
Where are LMN cell bodies located? How do LMN axons leave CNS?
brainstem (cranial nerve nuclei)
anterior horn of spinal cord

Axons leave CNS in cranial and spinal nerves
How many LMNs per muscle and vice versa?
Each LMN innervates several individual muscle fibers within a muscle.

Each individual muscle fiber is innervated by only ONE LMN
(During development, LMNs compete for muscle fibers, with only one winner per fiber)
What is a motor unit?
One LMN cell body in the CNS
It’s axon, branches, terminal regions
all of the muscle fibers it innervates
What type of damage is associated with fasiculations?
LMN
Why do fasiculations occur?
as the LMN cell body dies, it may fire spontaneously
(disorders of spinal roots may also do this)
causes its whole motor unit to twitch
visible to the naked eye
What are Deep Tendon Reflexes? What is the effect of LMN/UMN lesions? What is an inverse myotatic reflex?
Myotatic (muscle stretch) reflex = DTR
monosynaptic, detects muscle stretch (change in muscle length) through spindle and counters with muscle contraction (homonymous muscle)

DTRs lost with lesions of LMN (hyporeflexia or areflexia
because reflex circuit broken)

DTRs increased with UMN lesions (hypereflexia-
because UMN dampen DTRs usually)

Inverse myotatic- multisynaptic, detects muscle contraction through golgi tendon organ and counters with muscle relaxation- GTO detects tension
What is the other name for Monosynaptic Reflex (DTR)? What are the steps?
alpha-gamma coactivation

1.Muscle stretch activates Ia/II afferents. 2. Ia/II fibers activate LMN and muscle contracts. Also activate gMN which contract spindle fiber
When the muscle is stretched, what increases?
AP
What happens to AP during a - g Neuron coactivation?
constant
What can cause flaccid paralysis?
Acute UMN lesion occur rapidly
Flaccid paralysis = no muscle tone
The flaccid phase may last days to weeks to months…
complete loss of muscle tone, absent DTRs, absent plantar response (?)
or, with lesser lesion: weakness, hypotonia, hyporeflexia
When will a UMN lesion skip the flaccid period?
If lesion is subacute or chronic, this initial flaccid paralysis may not occur and hyperreflexive responses will prevail
What are the 4 main things from UMN damage?
hyperreflexia - due to loss of modulation of deep tendon reflexes.

clonus - rapid alternating contraction/relaxation of a stretched muscle – often more prominent in ankle reflex

clasp knife rigidity (“spastic catch”) - describes resistance to passive movement of a joint when
spasticity is present.
Muscles first resist the movement strongly ( DTR).
Then resistance melts away rapidly (GTO-based reflex kicks in)

spasticity - excessive muscle tone (hypertonicity), due to hyperactive stretch reflexes.
What neurogenic atrophy?
LMN damage
Potential Sites of Disruption of Motor Function
Upper Motor Neuron Cell Bodies
Projections from UMNs to LMNs
Lower Motor Neuron Cell Bodies
Projections from LMNs to Muscles
Presynaptic, ie Release of Transmitter from LMN Terminals
Postsynaptic, ie Receipt of Transmitter (ACh) By Muscles
Muscles
What causes ALS? What are signs and symptoms?
Amyotrophic lateral sclerosis (ALS)
Progressive degeneration of corticospinal tracts and a-motor neurons, both upper and lower MN disease. Absence of neurologic or organ system involvement and sparing of voluntary eye muscles and urinary sphincters
Symmetric gait disturbance, limb weakness, reflexes increased or depressed, dysarthia and dysphagia with respiratory complications
What is a neuropathy?
functional disturbances and/or pathological changes in PNS
What is Polyradiculoneuropathy?
affecting nerve roots
What are the major categories of peripheral neuropathy?
Major categories –
Inflammatory-AIDP
Hereditary-Charcot-Marie-Tooth Disease
Acquired metabolic & toxic (industrial or environmental chemicals)-Diabetic Neuropathy (DPN)
Traumatic (lacerations, avulsions, compressions (carpal tunnel syndrome and `Saturday night palsy´-ulnar nerve compression))
Infectious (e.g., leprosy, diphtheria, varicellar‑Zoster),
Associated with malignancy (invasion or paraneoplastic)
What is Acute inflammatory demyelinating polyradiculoneuropathy? What is it's other name? What initially causes it? What kind of damage, UMN or LMN? What are other signs and symptoms?
AIDP – (Landry-Guillain-Barré Syndrome)
40% “viral prodrome” (days to wks after URI or GI infection);
Causes acute paralytic illness
Clinical (acute):
Symmetrical glove/stocking paresthesia followed by leg weakness (several days)- and spreads up- ascending paralysis,
Pain –bilateral sciatica, or aching pain in thigh muscles and back (“Charley horse”)
Difficulty walking bilateral foot drop & unsteady waddling,
DTRs absent or reduced
Severe cases – respiratory distress
Eye movements, swallowing, and ANS functions affected
What is a Hereditary Motor and Sensory Neuropathies?
Charcot-Marie-Tooth Disease
Pes cavus-has high plantar arches with hammer toes and atrophy of foot muscles
Weakness/wasting in lower leg and foot producing “stork leg” (inverted wine bottle) (foot drop & stepped gait)
What Acquired Metabolic Neuropathy do we know? What are signs and symptoms? What part of the nervous system does it attack? What causes it?
Diabetic Neuropathy (DPN)
Distal sensory or sensorimotor neuropathy
symmetric polyneuropathies (pain, paraesthesias & weakness)
Autonomic neuropathy
Microvascular damage leads to DPN
What are 2 Peripheral Nerve Sheath Tumors?
Schwannomas (Arise from Schwann cells)
Acoustic neuroma = Vestibular Schwannoma
- tinnitus and hearing loss
large tumors - pressure on V & VII producing palsies, or brainstem compression & hydrocephalus

Neurofibromas (Arise from Schwann cells, perineural cells or fibroblasts)
Common cutaneous (Café au lait spots ‑ develop in childhood:
Lisch nodules ‑ small yellow/brown elevations), and peripheral nerve manifestations
What is the difference between pre and post synaptic Disorders of Neuromuscular Junction?
Presynaptic disorders are:
- frequently the result of a decrease in ability to release
neurotransmitter or the an uncontrolled release of
neurotransmitter until the terminal is depleted
- characterized by larger response with repeated stimulation
warm up phenomenon

Postsynaptic disorders are:
frequently the result of a decrease in availability of Ach
receptors on motor endplate.
characterized by fatigueability (smaller response with
repeated stimulation)
What is a presynaptic disorder?
Lambert-Eaton, blocks Ca+2 entry and ACh release
What causes Lambert Eaton? what are symptoms and treatment?
Cause:
Autoimmune disorder associated with non-neural carcinomas
Antibodies produced against VCCCs (voltage-dependent Ca++ channels)

Symptoms:
muscle weakness & fatigue (proximal) improves with exercise,
diminished reflexes
autonomic dysfunctions: dry mouth, impotence, hypotension

Treatment:
plasmaphoresis to remove IgGs, suppress immune system
Treat tumor
Death is more likely to result from associated cancer than from LEMS
What is the postsynaptic disease we learned of? Cause? Symptoms? Normal target?
Myasthenia Gravis muscle weakness occurs because circulating AChR antibodies cause increased degradation of Ach receptors

Few AChR on the muscle and Ach is broken down before it can stimulate the muscle resulting in muscle weakness
2/3 cases associated with thymic hyperplasia and 15-20% with
thymomas (rare neoplasm of the thymus -90% benign)


ptosis

20 year old females
What CNs are in the midbrain?
Pons? Medulla?
Midbrain: III and IV
Pons: V - VIII
Medulla: VIII - X, XII
What are the sensory cranial nerves of solitary tract, rostral and caudal?
rostral- CN VII, IX, and X
caudal- CN IX, X
What are the main cranial nerves with parasympathetics?
Edinger-Westphal- CN III
Abducens- VI
Nucleus Ambiguus- IX, X
What are the symptoms of CN III compression? What causes it?
What causes CN III ischemia?
CN III compression: eye down and out, pupil dilated, eyelid droop-
dilated unresponsive pupil early sign of CN III compression from temporal lobe herniation (because parasympathetic fibers are affected first)
CN III ischemia (Diabetes M) extraocular muscle palsy with pupil sparing
What are the CN of the corneal nerves?
sensory (CN V) and motor (VII)
What are the symptoms of a CN IV lesion?
IV Lesion- difficulty walking down steps, and reading b/c double vision ( posterior emergence) Come in with head tilt
What can cause CN VI damage? What are the symptoms?
VI (and III) susceptible to ICP
VI can not ABduct eye
What is the purpose of MLF? What can damage it?
MLF connects III and VI so you can have movement conjugate eye movement synchronized right and left eye movement (INO =damage MLF -think MS)
What controls the gag reflex?
Gag reflex= CN IX (sensory) CN X (motor)
What CN helps you rotate head and shrug shoulder?
XI
What is the effect of CN XII lesion? UMN versus LMN?
XII hypoglossal innervates ipsilateral tongue protrusion- LMN tongue deviates to side of lesion, UMN tongue deviates to opposite side. Each XII nerve directs tongue to opposite side. After damage the tongue deviates to weak side on protrusion that is towards LMN lesion and away from an UMN lesion
What handles taste sensation from the tongue?
Taste sensation from posterior 1/3 of tongue (IX)
Taste sensation from anterior 2/3 of tongue taste (VII)
What is a consequence of CN III lesion?
Eye position: down & out (downward & ABducted)
strabismus (eyes not directed towards same object)
diplopia (double vision)

Ptosis (lid droop)
Pupil dilation (mydriasis) and loss of accommodation
Accommodation = the process whereby the eye maintains a clear image (focus) of an object as its distance changes
A dilated and unresponsive pupil is an early sign of __________ lesion from a _____________?
Vascular lesions to this CN affect eye movement but spare ________.
CN III
temporal lobe herniation
because of parasympathetics goes first

pupils
Why is CN VI so susceptible to ICP?
Cranial Nerve VI has a very long run and is not very thick
How does abducens nucleus damage effect MLF (CL and IL)?
Damage to one abducens nucleus causes loss of LR ABduction in ipsilateral side and loss of contralateral eye ADduction (CN III MR)
What does damage to PRPF show (CL or IL)?
Damage to PPRF causes selective loss of rapid eye movements to ipsilateral side
What does damage to MLF cause regarding the MR?
Damage to one MLF causes selective weakness of the ipsilateral MR – can not ADduct during attempted lateral gaze
InterNuclear Opthalmoplegia (INO)
Where is the lesion? what is the symptom?
MLF
affects ipsilateral MR, contralateral LR
diplopia, affected eye (right) has impaired adduction, nystagmus in CL eye
What is nystagmus and what disease is it associated with in the eye contralateral to the injury?
Nystagmus: smooth pursuit in one direction, saccadic movement in other direction

INO
What lesion and muscle goes with the following symptoms?

Weak eye extorts
patient cannot look down & in
often becomes obvious when patient goes down stairs
Likely vertical diplopia
tilt head to good side to ‘fix’ diplopia (torticollis = twisted neck)
Trochlear and CN IV
What handles the Circuitry for Voluntary Saccades to each side?
FEF and Superior Colliculus Trigger Saccades to the Contralateral side
Why are smooth pursuits slower than saccades?
Tracking smooth pursuit movements (slower than saccades because uses visual feedback)
What causes Damage to Frontal Eye Field (right FEF)? What function is lost? What is redundancy?
Acute Stroke loose Right FEF. Possible “right gaze preference" due to unopposed left frontal eye fields activity.

NOTE: Redundancy- Eyes CAN move left as a tracking maneuver via a brainstem reflex
What is fixation?

What 2 reflexes are GAZE STABILIZATION?
Fixation = keeping the fovea pointed at the target of interest
Optokinetic reflexes:
keep the fovea on target during slow, sustained movements of head or target use visual feedback
Vestibulo-ocular reflexes:
keep the fovea on target during rapid & jerky head movements NO time for visual feedback! Use vestibular inputs
What is the point of the VOR?
Vestibular nuclei input
Allows us to generate eye movements equal and opposite to head movements- The VOR
Vestibulo-ocular reflex
What is connected in Saccadic Rapid eye movements? What is the purpose?
Fast
Connections between
the Frontal Gaze Center
to the PPRF

To bring new objects onto fovea
what is the connection in Smooth Pursuit movements? What is the purpose?
Slow
Connections from Parietal-Occipital gaze center via cerebellar and vestibular pathways

To keep a moving image
Centered on the fovea
what is the connection in . Vestibulo-ocular movements? What is the purpose?
Connections from vestibular system to the nuclei for motor movements

Keeps image steady on fovea during
head movement
what is the connection in Vergence movements? What is the purpose?
Optic Pathways to the oculomotor nuclei

To keep image in focus when moving near
What are the 2 components of the blink reflex?
Opthalmic division V1 of CN V, is the sensory component of corneal reflex and branch of VII nerve is the motor component
Blink Reflex Circuitry
Touching the cornea tests the integrity of CN V1 (nasociliary branch) and CN VII (contracts the orbicularis oculi muscles via the branchial motor division VII)
V lesion consequences?
Parethesia, neuralgia, hypo- or anesthesia one side of the face, disappearance of the corneal reflex, impaired mastication, mouth becomes oval
What are the symptoms of facial nerve damage (Bell's Palsy)? What can it be caused by?
He has lost control of muscles of facial expression:
He cannot wrinkle his forehead (effects both quadrants=LMN)
He cannot close his eye
He cannot smile symmetrically
Caused by herpes simplex I virus-may disappear spontaneously
Facial (CN VII) Lesions and their Consequences, what are the 2 types?
UMNL (upper motor neuron lesion) Supranuclear (cortex)
Contrlateral effects on
lower quadrant only
Upper quadrant receives
input from both hemispheres
Whereas lower quadrant
only contralateral input


LMNL (Lower motor neuron lesion) Lesion of facial nucleus or more peripheral
Ipsilateral effects on both upper and lower quadrants of the face
How is control of the upper and lower face organized?
Upper face is controlled bilaterally from the cortex;
Lower face is controlled only from the contralateral cortex
Why is the Forehead unaffected, in UMN lesion of CN VII?
bilateral cortical control
What functions do IX and X share?
control of speech and swallowing
Where do the branchial motor components of IX and X originate?
nucleus ambiguus in the medulla
When is DCML contralateral and ipsilateral?
CL: cortex to rostral medulla
IL: Spinal cord, all
How are the primary, secondary, and tertiary neurons split in the DCML?
Primary sensory neurons
Axons ascend in posterior funiculus
bundle = posterior columns
Fasciculus gracilis (leg)
Fasciculus cuneatus (hand) lateral
synapse in medulla
Second order sensory neurons
Cell bodies in
Nucleus gracilis
Nucleus cuneatus lateral
Axons cross midline as internal arcuate
Axons ascend to thalamus as medial lemniscus
Third order sensory neurons
Cell bodies in VPL of thalamus
Axons join internal capsule to project to primary (and secondary) somatosensory cortex
What is the purpose of the DCML?
proprioception, fine touch, vibration
How do we test proprioception?
Move big toe up and down (hold on sides of toe)
And the Romberg test
What causes a positive Romberg test?
Problem with DCML, OR a problem with afferent sensory information
What is the pathway of the STT/ Anterolateral system?
1˚ afferents (ascend or descend for 2-3 segments ) synapse on second order neurons (PTN)
Cross the midline in anterior white commissure of spinal cord
PTN axons ascend in the anterior portion of the lateral funiculus as the anterolateral system
STT transmits information from the spinal cord to the VPL of the thalamus
to Somatosensory cortex
What are 3 diseases/deficiencies that cause DCML damage?
MS, Syphilis, and Vit B deficiency
What is Bilateral INO pathognomonic for?
MS
If a hit to the spinal cord is at the cervical level, what effect will it have on the STT and DCML of the leg?
CL STT loss
IL DCML loss
In the spinal cord, is the CST ipsilateral or CL?
ipsilateral, crosses at medulla
Cause:
Ipsilateral spastic paralysis and loss of vibration, fine touch and proprioception
And
contralateral loss of pain and temperature
beginning one or more segments below the level of damage
Spinal cord damage
Damage to the cervical spinal cord causes what loss?
causes loss of control of ipsilateral sympathetic preganglionics, resulting in a partial Horner syndrome- Miosis and ptosis affecting the contralateral eye
Where do sympathetics of the eye emerge?
fibers emerge at about T1 and ascend in the sympathetic trunk to synapse in the superior cervical ganglion
What is Horner's syndrome and what can cause it?
Ipsilateral to lesion
Loss sweating
Pupil constriction and
lid droop

Damage sympathetic out-flow to face-
Hypothalamus
Brainstem (Lat Med Syn)
Cervical spinal cord- interrupts descending control or affects sympathetic preganglionic cell bodies
Ascending Symp. Trunk (apical lung tumor)
Postganglionic symp. Fiber damage (Carotid artery aneurysm)
What is Syringomyelia and what does it cause?
a central cavity in the spinal cord

SST (anterolateral sytem) Anterior White Commissure Hit

Severe burns- Analgesia and thermanesthesia in both hands -segmented and bilateral -sensory motor ok in legs, Proprioception OK, Fasciculations in both arms (LMN)
Typical findings include: a band of bilateral loss of pain and temperature sensation, and can have weakness and atrophy if damage extends to the anterior horns
syringomyelia
SPLIT – Dissociated Senses
Where is lesion?

-Loose pain sensation from CL- right foot, without loss of vibratory sense from right foot. Will loose vibratory sense from ipsi -left foot.
Thoracic level left half of spinal cord
Where is this lesion:
Lose pain sensation from CL -right foot, & lose vibratory sense from CL-right foot?
Brainstem damage exclusively on the left side
What is the role of basal ganglia?
Role of Basal Ganglia is to Select and Suppress Movements-

Selection & initiation of willed movements , and suppression of unwanted movements
What are the 2 pathways of the basal ganglia?
The Direct Path releases thalamic activity
This results in increased thalamic activity and increased motor output (Because caudate & putamen inhibit SNr/Gpi)

The Indirect Path inhibits thalamic activity
This results in decreased thalamic activity, and decreased motor output (Because of increased BG output (SNr/GPi)
Parkinson’s involves loss of what pathway and what are the symptoms?
Loss of Da Producing Neurons in Substantia Nigra -Striatal Pathway

Tremor (resting)
Rigidity
Akinesia (hypokinesia, bradykinesia)
Posteral instability (flexed posture- Festinating gate)
-Dementia

Difficulty getting out of a chair, fall backwards, Cogwheel rigidity, Stiff gate stooped posture, no arm swing, short shuffling steps,
Festinating Gate = accelerate the further they walk
What diseases look like Parkinson's?
Parkinson’s Disease
Diffuse Lewy Body Disease
Drug Induced Parkinson’s -MPTP (synthetic heroine contaminant), -Reglan (antinausea medication), -Haldol (antipsychotic medications)
Post Traumatic Parkinsonism
What is Huntingtons Disease?
inherited disease
CNS

progressive dementia
involuntary choreic movements

degeneration of the caudate and putamen nuclei
What causes dementia and chorea in HD?
dementia (characterized by both cognitive and personality changes) in HD is caused primarily by the degeneration of neurons in the cerebral cortex, and the chorea is caused by degeneration in the basal ganglia
What are the 4 C's of HD?
chorea
CAG repeats
caudate
cortex
Hemiballismus:
What is hit? Symptoms?
Subthalamic Nucleus Hit
Contralateral unintentional, forceful flinging movements of the right arm and leg (or rotatory in nature)
Dystonia
Persistence of a postural abnormality, a sustained posture or position of any part of the body
Wilson Disease

What is it? What is the hallmark? What is it associated with? What is it caused by? Symptoms? Treatable?
Disorder of Copper Metabolism Affecting Brain & Liver

Kayser-Fleischer ring (copper-colored ring around cornea)

Associated with a decrease in ceruloplasmin concentration (a blue plasma copper transport protein)

Genetic (leads to hepatolenticular degeneration)
Movement disorders include: dystonia, tremor, chorea, rigidity & other BG-related signs
TREATABLE!
What is the function of the cerebellum?
Proper execution of planned motor acts
Establishes direction, timing , force of planned
motor acts
Compares intended movements with ongoing movement
Involved in motor learning
What are the cerebellar tests?
Finger to nose
Heel-knee-shin test
Rapid alternating movement
(Dysdiadochokinesia = inability to perform
rapid, alternating movements)
Gate examination
Alternating pronation-supination test
Is cerebellar dysfunction ipsilateral or contralateral?
ipsilateral
What are the symptoms of Cerebellar Dysfunction-IPSILATERAL?
Intention Tremor -during planned motor activity
(ie reaching for target)
Hypotonia- loss resistance
Disequilibrium- loss balance, gate and trunk
dystaxia- jerky, irregular, arrhythmic movement s

Dyssynergia- loss coordination, dysmetria, nystagmus.
Abnormalities in:
- rate of movement = initiation & mvt slowed,
- direction or range of movement
- force of movement (hypotonia)

Ataxia- uncoordinated, voluntary movement
Where does “Alcoholic” Cerebellar Degeneration attack? What are the symptoms? What is a probable cause?
Superior vermis more affected than hemispheres
Gait ataxia without limb ataxia
Probably a problem relating to malnutrition
What are the Monoaminergic pathways?
Serotonergic pathways from several raphe nuclei: project widely rostrally and caudally

Norepinephrine pathways from Locus ceruleus
and Lateral tegmental area : project widely rostrally and caudally

Dopaminergic pathways from the Substantis nigra pars compacta (SNc) and the ventral tegmental area (VTA) : project to striatum
Where does the serotonergic pathways project from and where to?
Serotonergic pathways from several raphe nuclei: project widely rostrally and caudally
Where are norepinephrine pathwaws run and where do they project?
Norepinephrine pathways from Locus ceruleus
and Lateral tegmental area : project widely rostrally and caudally
Where does the dopaminergic pathway come from and where do they project?
Dopaminergic pathways from the Substantis nigra pars compacta (SNc) and the ventral tegmental area (VTA) : project to striatum
What NTs affect sleep?
Sleep function is altered by
Norepinephrine (arousal)
Serotonin (promotes sleep)
Dopamine (arousal)
Acetylcholine (in cortex – arousal)
Histamine (arousal)
GABA (promotes sleep)
Opioid/opiates (promote sleep)
What does the Electroencephalogram (EEG) measure?
EEGs Measures cortical electrical activity, EPSPS and IPSPS summed from cortex
What are the characteristics of a normal EEG?
Alert with eyes open = asynchronous, low voltage, fast activity EEG
What are the stages of sleep?
stage 1: Theta rhythms
stage 2: Sleep spindles
stages 3 and 4: Delta rhythms
Stage 5: During REM sleep, the EEG displays a beta rhythm, which is characteristic of the waking state
What is the deepest nonREM stage?
stage 4
SWS versus REM?
Deep Slow Wave Sleep
Difficulty waking
No eye movement
Parasympathetic control dominates (slowed HR)
Sleep deprivation causes
increased stage 4 sleep
Stage 4 suppressed by valium
Sleep walking (somnambulism)


REM
Rapid Eye Movement
High freq, low voltage
similar to awake beta wave
Deepest sleep of all
Atonia (muscle paralysis)
Wake spontaneously
Sympathetic activity dom.
Vivid dreaming
Suppressed by alcohol, barbiturates, TCAs
What is insomnia?
Subjective sense of insufficient sleep. Inability to achieve sufficient sleep or difficulty in falling asleep (>30 min). A symptom, not a disorder per se
What causes insomnia?
Anxiety / depression / stress / pain
Side effect of meds / alcohol / poor sleep habits?
Disruption of circadian rhythms?
Increasing age?
What are the effects of insomnia?
Problems with memory & concentration
Potential link with cardiovascular disease
4-fold increase in likelihood of depression
Impaired performance (at home, on the job, driving)
What is Obstructive Sleep Apnea?
What is is accompanied by and more common in? What is sleep apnea?
Obstructive sleep apnea is the major cause of daytime sleepiness up to 500 awakenings per night!

heavy snoring

overweight individuals (physical abnormalities of neck, throat).

Sleep apnea = brief periods of interrupted breathing during sleep
What is Narcolepsy?
Enter REM sleep directly from the waking state

Excessive daytime sleepiness ((EDS) “sleep attacks” = abrupt transition to NREM sleep

Cataplexy -sudden loss of muscle tone in awake state

Hallucinations while falling or awakening from sleep and suffer from sleep paralysis(awake but can’t move for several minutes)

Narcolepsy is associated with a lack of orexin (hypocretin- a hypothalamic protein)- genetic or autoimmune-related neurodegeneration
What is the purpose of Reticular Formation Functions?
Activates the cerebral cortex (arousal and wakefulness)
Integrates cranial nerve reflexes
Modulates pain – intrinsic analgesic system
Influences voluntary movements
Regulates autonomic nuclei
Integrates respiration and sleep
What does Consciousness involve? Where?
1. Alertness
(pontomesencephalic RF, thalamus and cortex)
2. Attention
(same circuits as above plus frontoparietal
association cortex)
3. Awareness
higher-order integration of multiple brain regions
What causes Persistent Vegetative State? What still functions? What is preserved? What about spontaneous eye movements? What is missing?
Cause: severe, diffuse cerebral cortical damage with brainstem function intact (“cerebral death”)
Respiratory system, circulatory system functioning
Possible preservation of sleep-wake cycle on EEG
Spontaneous eye movements
but NO evidence of awareness / responsiveness / interaction with environment
NO meaningful responses
How is a vegetative state different from coma?
After several weeks of being in a coma a patient
may emerge into a state in which they regain
sleep-wake cycles and other primitive orienting
reflexes mediated by the brainstem and
hypothalamus, but remain unconscious
What happens in a coma over six hours in length?
diffuse axonal injury
What is coma not?
Not sleep, which is readily reversible
Not fainting/syncope, which is transient
Not Inattention/Confusion/Stupor
Where is there decorticate and decerebrate posture? Flaccid paralysis? Death?
Above midbrain

Midbrain (red nucleus)

Pons

Medulla
The UMN Pathways that Originate in the Brainstem
Tectospinal- reflex head turning
a Rubrospinal- arm flexor bias
arm flexion seen in decorticate rigidity stems from unopposed
rubrospinal tract activity.
Reticulospinal- feed- forward extensor bias
Vestibulospinal-
feed-back adjustments
arm and leg extension bias
due to unopposed vestibulospinal tract activity – seen in decerebrate rigidity
Of the UMN pathways that originate in the brain, which on is seen in decorticate and which is seen in decerebrate?
Rubrospinal- arm flexor bias
arm flexion seen in decorticate rigidity stems from unopposed rubrospinal tract activity.

Vestibulospinal- feed-back adjustments
arm and leg extension bias due to unopposed vestibulospinal tract activity – seen in decerebrate rigidity
What does a score of 0 and 15 mean on the Glasgow scale?
0 = death
15 = okay
Respiratory Patterns and Levels of Lesions in Coma
1. Deep forebrain—Cheyne-Stokes
2. Midbrain—central neurogenic hyperventilation
3. Rostral pons—apneustic
4. Midpons—cluster breathing
5. Caudal pons or rostral medulla—ataxic breathing
6. Respiratory centers in mid-medulla—respiratory arrest
Clinical Examination to Assess Brain Death
step 1, check motor response and check the eyes do not open when a painful stimulus is applied to the supraorbital nerve or nail bed.

step 2, Assess brain-stem reflexes
Absence of grimacing or eye opening with deep pressure on both condyles at the level of the temporomandibular joint (afferent nerve V and efferent nerve VII), the absent corneal reflex elicited by touching the edge of the cornea (V and VII), the absent light reflex (II and III), the absent oculovestibular response (VIII and III and VI), and the absent cough reflex elicited through the introduction of a suction catheter deep in the trachea (IX and X).

Step 3, apnea test , disconnect the ventilator -observe and monitor the patient for changes in vital functions
What brain stem reflexes do you check for in brain death?
grimacing or eye opening –apply deep pressure on the temporomandibular condyles (afferent V & efferent VII)

corneal reflex - touching the edge of the cornea (V and VII)

light reflex (II and III)

oculovestibular response (VIII and III and VI)

gag reflex – push suction catheter deep in the trachea (IX and X)
Match cause of coma to pupils:

toxic or metabolic

midbrain lesion or transtentorial herniation

pontine lesion

opiate overdose, pontine damage
Toxic or metabolic- normal sized, reactive

Midbrain lesion or
Transtentorial herniation-Unilateral or bilateral blown pupil

Pontine lesion- Small, responsive to light bilaterally

Opiate overdose, Pontine damage- Bilateral Pinpoint pupils
What is the normal VOR? What can explain its absence?
The oculocephalic reflex is present if the eyes move in
the opposite direction of the head movements (doll’s eyes)


brainstem dysfunction in coma, or barbiturate overdose, but can be normal in awake state (normal eye movements)
Caloric Testing, indicate the lesion:

Cold Water in Ear --> smooth conjugate eye turn to ipsilateral side and stay

cold water in ear --> deviation to side cold water with nystagmus in opposite direction

cold water --> 1 eye does not adduct on spontaneous eye movements or in response to reflex maneuvers
intact brainstem, damage to supratentorial cerebrum

normal

INO
What are the necessary preconditions for brain death?
acute catastrophic brain injury must be present
Rule out all reversible causes: No hypothermia (BT > 90˚ F or 32˚ C), No drug-related cause, No shock
What are the tests for brain death/coma?
no response to verbal or visual command
no movement in response to painful stimuli
Absent brainstem reflexes-pupils mid-position and nonreactive,absent corneal reflex, absent oculocephalic (“doll’s eye”) reflex, or absent VOR on caloric test), absent gag reflex
Apnea: no spontaneous ventilation
EEG is done to confirm brain death- it shows “electrocerebral inactivity” (flat pattern, < 2mV in amplitude)
What is the difference between coma and brain death?
brainstem reflexes and non-flat EEG (various fixed patterns)
How is persistent vegetative state different from coma?
presence of sleep wake cycles
What is the different between locked in syndrome and coma?
Eye movements and blinking. Locked in is lesion to anterior pons. that spares CN VII. Also, normal EEG.
What are simple vs complex partial seizures?
Simple Partial Seizures- small local but progress to generalized
vague location, Aura-auditory or visual hallucinations, emotional experience, arms, legs or face may twitch. Does not impair consciousness
Complex Partial Seizure (psychomotor or temporal lobe)
Altered consciousness, Sensory, motor and ANS symptoms, some have aura (unpleasant odor or taste), Start blank stare, post-ictal- somnolence or confusion, with no recollection of seizure
What is a partial seizure?
Involves a limited portion of the brain
Starts on one side (foci = start location)
What is a Jacksonian march?
progression of seizure location with march of symptoms a -start in feet and legs goes to arms hand and face
Generalized Seizures
Not localized to one area (no aura)
Travel throughout entire brain on both sides
Originates bilaterally and symmetrically
Define the following seizures:

absence
myoclonic
tonic clonic
atonic
Absence (petit mal) Occur in children, last seconds, loss of activity and not responsive
Myoclonic large jerky movements
Tonic clonic- LOC-alternating intense contraction and relaxation, hoarse cry out, post ictal may sleep, confused, sore
Atonic (drop attacks)
Status Epilepticus:
Continuous series of seizures without reawakening
generalized seizure consisting clinically of a brief staring spell in conjunction with a characteristic burst of spike-wave complexes on the EEG
Absence Seizure
What is a generalized seizure?
Both hemispheres hit – NOT local
What nerves are parasympathetic?
sympathetic?

Note: nerves denote PNS, so the question is really asking, where does parasympathetic CNS become PNS.
CN (III, VII, IX, X) & S2-S4

T1-L2
Describe the pre and postganglion action and NT of somatic efferent and the autonomic.
Somatic efferent cell bodies in the CNS release Ach onto target skeletal muscle expressing nicotinic Ach receptors.
The ANS innervates smooth muscle, gland cells and cardiac muscle. Sympathetic preganglionic fibers with cell bodies in the CNS release ACh onto postganglionic neurons expressing nAChR.
Postganglionic axons release NE on target smooth and cardiac muscles expressing a and b-adrenergic receptors.
Parasympathetic preganglionic fibers with cell bodies in the CNS release Ach onto target smooth and cardiac muscles expressing mAChRs.
What 2 actions occur when successfully urinating?
contract detrusor, relax sphincters
What control the bladder?
Several regions of cerebral cortex (prefrontal) for voluntary override
Pontine micturition center (Barrington’s nucleus) via the reticulospinal tract for general coordination (similar to UMN)
Sympathetic (T10-L2) to STOP
Innervation of base of bladder (trigone, neck, internal sphincter) through hypogastric nerve
Parasympathetics (S2-S4) to PEE
Innervates dome of bladder through pelvic nerve
Somatic motor (S2-S4) to Stop voluntarily
“Lower motor neuron bladder” indicates a lesion of sacral spinal cord or cauda equina. What are the clinical symptoms?
no parasympathetic ability to initiate micturition = no voluntary control of external sphincter
Detrusor flaccid = large bladder, poor emptying
Sphincter has decreased tone = overflow incontinence (cannot withstand additional pressure)
Bladder fills to max capacity, then dribbles,
urinary retention
overflow incontinence
“Lower motor neuron bladder”
“Upper motor neuron bladder”

Where is the lesion? What are the symptoms?
Following loss of input from pontine micturition center, i.e. anywhere between pons and S2 (start of parasympathetic output to bladder)
Similar to other UMN lesions, associated with hyperactivity:
small, spastic, hypertonic bladder that empties reflexively (1-4 hr), but may not FULLY empty
increased sphincter tone? Difficulty initiating stream
When do you have to catheterize a patient with nerve damage to bladder?
During the period of spinal shock immediately following injury, one sees atonic bladder
“uninhibited bladder”
Loss of cortical input
Leads to urinary incontinence,
but no urinary retention problem because detrusor-sphincter loop is still intact
Urination: Micturation reflex
Stretch receptors fire

Parasympathetic neurons fire

motor neurons stop firing

Smooth muscle contracts
Internal sphincter passively pulled open.

External sphincter relaxes
what 4 functions of homeostasis does the hypothalamus control?
Blood pressure
Body temperature
Fluid and electrolyte balance, and
Body weight
What does the Anterior hypothalamic nuclei control? What does a lesion lead to?
heat dissipation center; triggers sweating, cutaneous vasodilation. (think Anterior Center = AC)
Estrogen receptors! Hot flashes??
Lesion leads to hyperthermia - inability to dissipate heat. Potentially fatal!
Posterior hypothalamic nuclei

What is its purpose and what does a lesion lead to? What kind of lesion?
heat conservation center, triggers cutaneous vasoconstriction and heat production center, triggers shivering
Bilateral lesion
inability to raise core temperature (heat production/conservation)
may result in complete loss of ability to thermoregulate (poikilothermia)
What are the Anorexic neuropeptides
that act on the hypothalamus?
Alpha MSH, cocaine and amphetamine related transcript (CART) prooplomelanocortin (POMC)
Orexigenic Neuropeptides
Neuropeptide Y, agout-related peptide (AgRP) Orexins (hypocretins)
What are the Signals from the periphery that cause anorexia?
Leptin (adipose), Insulin, Ghrelin, glucocorticoids
Leptin

What does it do? What happens in its absence? Where are receptors?
Hormone produced in adipose tissue-product of the ob gene
Leptin infusion into 3rd ventricle inhibits food intake and energy expenditure
Absence of circulating active leptin results in obesity, diabetes and sterility
Abundent leptin receptors in VMN and lateral hypothalamus
What lesion is indicated by loss of a consensual pupillary light reflex?
CN III
What lesion is indicated by loss of a direct pupillary light reflex?
CN II
What lesion is indicated by a complete lack of pupillary light reflex?
CN II
For the cochlear nerve, what will the following result in:

destruction
irritative lesions
deafness

tininess
Acoustic neuroma (schwannomma)
schwann cell tumor of the cochlear nerve that causes deafness and…
What are the full side effects of an acoustic neuroma?
Auditory (VIII):
tinnitus, ipsilateral deafness
Vestibular (VIII):
vertigo/dizziness, nausea, nystagmus
Facial (VII): multiple findings
ipsilateral facial paresis/paralysis, loss of corneal reflex,
loss of taste (front 2/3 of tongue),
loss of salivation, tearing
hyperacusis? No! overridden by deafness!
Cerebellar signs possible
What Regulates compensatory eye movements (to head movements)?
vestibulocochlear nerve
What nerve is associated functionally with the cerebellum (flocculonodular node) and oculomotor nuclei?
vestibulocochlear nerve
First order sensory bipolar cells in the vestibular ganglion (internal auditory meatus) project to the hair cells of the cristae of the semi-circular canals, and to the hair cells of the uticle and saccule
They also project to the vestibulo nuclei of the brain stem and flocculonodular lobe of the cerebellum

Which nerve?
Vestibulocochlear nerve
What are the utricle and saccule sensitive to?
Uticle sensitive to tilts beginning from upright and responds to acceleration in the horizontal plane, the saccule is sensitive to tilts from sideways position and accelerations in the vertical plane
What does a Vestibulocochlear nerve
lesion cause?
Disequilibrium,
Vertigo, and
Nystagmus (nystagmus can be physiological or pathological)
What are the 2 forms of deafness?
- those that impair the ability of airborne vibrations to reach the organ of Corti (Conductive hearing loss- eg from middle ear infection) only affects ability to hear sounds delivered in air (no effect on skull vibrations) so impaired hearing in one ear by air conduction but normal hearing by bone indicates conductive hearing loss
- those that impair the ability of hair cells or the cochlear nerve to respond (sensorineural hearing loss) Damage from noise exposure or VIII tumor result in impaired hearing no matter what route used to deliver vibrations
What are the three kinds of deafness and the causes attributed?
Conductive Hearing Loss
External ear obstructions (wax?, peas?)
Middle ear obstructions: Otitis
Otosclerosis - commonly causes progressive hearing loss

Sensorineural Hearing Loss
Degeneration of hair cells
Presbycusis (high freqs go first: 20,000 down to 8,000 or 4,000 Hz)
Lesion of cochlear nerve

Central Hearing Loss
Lesion of primary auditory cortex (Brodmann's areas 41 and 42)
Lesion of Wernicke's area (Brodmann's area 22)
Seizure activity in the auditory cortex (e.g. temporal lobe epilepsy)
Tinnitus = the paresthesia of the auditory system
How do you diagnose conductive hearing loss with the weber test? Sensineural?
Louder in the bad ear (the conduction problem masks the ambient noise of the room)

Louder in good ear (the affected ear is less effective at picking up sound even if it is transmitted directly by conduction into the inner ear)
How do you diagnose conductive hearing loss with the rinne test? Sensineural?
In both cases, with the good ear, AC > BC

With conductive BC > AC with the bad ear (bypasses bad conduction)

With sensineural AC > BC (bypass doesn't matter)
Meniere's disease (VERY IMPORTANT)
hearing loss and vertigo due to alteration in endolymph pressure (increase)
What is the difference between dementia and delirium? (Hint: What does David Wong love?)
attention (demented people can still attend to you)

onset (dementia is slower)
What are the symptoms and treatment of normal pressure hydrocephalus?
Confusion, depression, problems with memory, urinary incontinence and ataxia- worse over a period of weeks

- shunt to divert CSF can reverse the dementia
Alzheimer’s Disease (AD)

definitive diagnosis

symptoms
Definitive diagnosis of AD requires postmortem
examination of the brain and sufficient numbers of
plaques and tangles to qualify as affected by AD


progressive memory impairment
- disordered cognitive function
- altered behavior, including paranoia and delusions
- progressive decline in language function
What are extracellular and intracellular with alzheimer's?
extracellular- plaques
intracellular- tangles
What genotype is protective and which is harmful for alzheimers?
ApoE2
ApoE4
What neurochemistry occurs in alzheimers?
50-90% decrease in choline acetyltransferase activity in cerebral cortex and hippocampus – selective loss of ACh neurons (from deep nuclei in septum to hippocampus and basal nucleus of Meynert to the cerebral cortex)


Glutamate may be involved in loss of large neurons in both cortex and hippocampus
Severely enlarged ventricles, cortical & hippocampal shrinkage
AD
What are the general functions of the different areas of the brain?
Frontal lobe: personality and higher centers for voluntary motor activities (Primary motor cortex- seen in red)
Parietal lobe: peripheral sensations (primary somatosensory cortex- seen in blue)
Temporal lobe: sensations of smell, taste (in insula) & hearing
Occipital lobe: vision
What are the parts of the Limbic lobe and their function?
Hippocampus-involved in memory, and damage results in amnesia
Amygdala is involved with fear and anger and the emotional interpretation of events and visual stimuli
Anterior cingulate gyrus -pain
What is active during emotional interpretation of visual stimuli?
amygdala
Hyperalgesia
definition and types?
Increased response to painful inputs
Primary hyperalgesia: Increased sensitivity to pain with lowered threshold at mechanical and thermal nerve endings

Secondary hyperalgesia: Changes within CNS that cause increased response by
[1] lowering the threshold or
[2] increasing its magnitude of pain evoked by suprathreshold stimuli.
Allodynia
pain resulting from a normally non-nociceptive stimuli
Pain can be modulated
at the brainstem and at the spinal cord dorsal horn
Endogenous Pain Control Mechanisms
Enkephalinergic interneurons within the dorsal horn can inhibit pain transmission
Noradrenergic projections from pontine centers terminate on neurons and terminals within the dorsal horn and inhibit pain transmisssion
Activation of cannabinoid receptors in the spinal cord dorsal horn can limit pain
Serotonergic projections from brainstem raphe nuceli can activate local circuits within the dorsal horn of the spinal cord to prevent pain transmission
Endogenous opioids
Visceral Pain: Summary
Visceral nociceptors respond to mechanical stretching (distention), ischemia, chemicals released by tissue damage (H+, bradykinin, PGE2, etc)
Visceral pain transmitted to spinal cord primarily bundled in sympathetic afferents (T1-L2)
Visceral pain: poorly localized
Visceral pain may be referred to associated somatic region
Referred Pain
Pain of visceral or parietal origin may be perceived as somatic pain by the patient.

The somatic region to which the pain is referred is always a dermatome(s) that is (are) innervated by the same dorsal roots that supply the irritated structure.

Thus the site of the referred pain can direct the clinician to appropriate underlying visceral sources.
Concerning the STT tract in the medulla, is it CL or IL with the pain, temp, and crude touch from the face?
Ipsilateral
What infarct causes a hearing loss?
AICA
What is Parinaud syndrome?
compression of posterior midbrain

Vertical gaze center- Loss vertical gaze, eyes deviate downward

Vergence center- Nystagmous on eye convergence

Posterior commissure
and tectum- Loss pupillary light response, possibly with accomidation intact
Who is at a higher risk of tearing bridging veins? What type of aneurysm?
alcoholics and elderly
subdural
What is contained within medullary pyramids?
CST axons