Neuroanatomy Flashcards
Frontal lobe cortices
(Anterior to posterior)
1. Prefrontal cortex
2. Frontal eye fields
3. Premotor cortex
4. Primary motor cortex
Prefrontal cortex subregions
- Dorsomedial – behavioral activation (bilateral damage: apathy/mutism)
- Dorsolateral – cold EF, can also see apathy (damage: dysexecutive syndrome), persistence, perseverative errors on WCST
- Ventromedial – Hot EF, risk and fear (regulates limbic activity) (damage: disordered reward/punishment processing)
- Orbitofrontal – Hot EF, (damage: disinhibition)
“Hot core” of prefrontal region (orbital frontal and ventral medial) everything else “cold”
Cranial nerve name mnemonic
On (olfactory - smell)
Old (optic - vision)
Olympus’ (oculomotor - eye movement)
Towering (trochlear - eye movement)
Top (trigeminal - face sensation)
A (abducens - eye movement)
Fiercely (facial - motor to face)
Villainous (vestibulocochlear - balance and hearing)
German (glossopharyngeal - swallowing and taste)
Viewed (vagus - parasympathetic)
Some (spinal accessory - shoulder shrugging)
Hops (hypoglossal - tongue movement)
Cranial nerve function mnemonic
Some - olfactory (sensory)
Say - optic (sensory)
Marry - oculomotor (motor)
Money - trochlear (motor)
But - trigeminal (both)
My - aducens (motor)
Brother - facial (both)
Says - vestibulocochlear (sensory)
Big - glossopharyngeal (both)
Brains - vagus (both)
Matter - accessory (motor)
More - hypoglossal (motor)
Describe corticospinal tract route
Begins in the primary motor cortex and projects downward through white matter and brainstem
85% of fibers cross over (“pyramidal decussation”) at junction between medulla and spinal cord to control movement opposite side of body
Lesions above decussation produce contralateral (opposite side) weakness
Lesions below decussation produce ipsilateral (same side) weakness
Two main sensory pathways
• Posterior column pathways – convey proprioception, vibration sense, and fine discriminative touch
o Enter spinal cord via dorsal roots and columns to dorsal column in medulla (ipsilateral)
o Cross over to the other side of medulla
o Continue to ascend on the contralateral side and synapse in the thalamus
o Neurons then project to the primary somatosensory cortex
• Anterolateral pathways – convey pain, temperature sense, and crude touch
o Enter spinal cord via dorsal roots and synapse in spinal cord gray matter and cross over to other side of spinal cord
o Ascend in the anterolateral white matter, which forms the spinothalamic tract
o Synapses in the thalamus
o Continues to the primary somatosensory cortex
Limbic system structures
hippocampal formation, amygdala, limbic lobe (parahippocampal area and cingulate cortex)
Limbic system damage
• Lesions in the limbic system can cause deficits in the consolidation of immediate recall into longer-term memories. Thus, patients with lesions in these areas may have no trouble recalling remote events but have difficulty forming new memories.
• In addition, limbic dysfunction can cause behavioral changes and may underlie a number of psychiatric disorders.
Limbic system seizures
Epileptic seizures most commonly arise from the limbic structures of the medial temporal lobe, resulting in seizures that may begin with emotions such as fear, memory distortions such as déjà vu, or olfactory hallucinations.
Gerstmann’s syndrome
Lesions in the inferior parietal lobule in the left hemisphere can produce a constellation of abnormalities:
- difficulty with calculations
- right–left confusion
- inability to identify fingers by name (finger agnosia)
- difficulties with written language.
Describe the three fossae (i.e., compartments of the cranial cavity)
• The anterior fossa on each side contains the frontal lobe.
• The middle fossa contains the temporal lobe.
• The posterior fossa contains the cerebellum and brainstem.
Location of ventricles
• There are two lateral ventricles (one inside each cerebral hemisphere)
o have extensions called horns that are named after the lobes or after the direction in which they extend
- frontal horn
- occipital horn
- temporal horn
• third ventricle located within the thalamus and hypothalamus
• fourth ventricle located within the pons, medulla, and cerebellum.
Intracranial mass lesions can cause neurologic symptoms and signs by the following mechanisms:
- Compression and destruction of adjacent regions of the brain
- A mass located within the cranial vault can raise the intracranial pressure
- Mass lesions can displace nervous system structures so severely that they are shifted from one compartment into another (i.e., herniation) such as a midline shift
Symptoms and signs of elevated intracranial pressure
• headache – usually worse in the morning
• altered mental status (irritability, reduced alertness)
• nausea and vomiting
• papilledema – engorgement of optic disc
• visual loss
• double vision (aka diplopia)
• Cushing’s triad – hypertension, bradycardia, irregular breathing
Describe three herniations
• Tentorial/uncal herniation – herniation of the medial temporal lobe, especially the uncus (medial lobe), that pressed on CN 3
o Clinical triad: “blown” pupil (generally dilated pupil is ipsilateral to lesions), hemiplegia (usually weaker side is contralateral to lesion if corticospinal tract is affected above pyramidal decussation in the medulla), and coma
• Central herniation – central downward placement of the brainstem
• Subfalcine herniation – results from shift of cingulate gyrus; no clear clinical signs
What is a herniation?
Occurs when mass effect (i.e., distortion of normal brain geometry due to a mass lesion) is severe enough to push intracranial structures from one compartment to another
Severe head trauma can cause permanent injury through:
• diffuse axonal shear injury, which causes wide- spread or patchy damage to the white matter and cranial nerves;
• petechial hemorrhages, or small spots of blood in the white matter;
• larger intracranial hemorrhages
• cerebral contusion (bruise on the brain)
• direct tissue injury by penetrating trauma such as gunshot wounds or open skull fracture.
• Cerebral edema (swelling) may occur as well, with or without other injuries, contributing to elevated intracranial pressure in head injury.
Four types of intracranial hemorrhage
• Epidural hematoma (EDH) – between dura and skull, usually caused by fracture of temporal bone
• Subdural hematoma (SDH) - between dura and arachnoid
• Subarachnoid hemorrhage (SAH) – in CSF-filled space between the arachnoid and the pia, which contains the major blood vessels of the brain
• Intracerebral or intraparenchymal hemorrhage (ICH) - Within the brain parenchyma in the cerebral hemispheres, brain- stem, cerebellum, or spinal cord.
Hydrocephalus is excess CSF in the intracranial cavity due to:
• excess CSF production – rare cause; seen only in certain tumors
• obstruction of flow at any point in the ventricles or subarachnoid space – common cause due to infection, inflammation, prior hemorrhage, etc.; caused by congenital malformation or obstruction by tumors and masses, most likely in the narrow points of the CSF flow path:
o foramen of Monro – channel between lateral ventricles and third ventricle
o cerebral/Sylvian aqueduct – channel between third ventricle and fourth ventricle
o fourth ventricle – located posterior to pons and upper medulla & anterior to cerebellum
• decrease in reabsorption via the arachnoid granulations – same cause of obstruction
Where is CSF produced and absorbed?
produced in the choroid plexus (within the lateral, third, and fourth ventricles)
reabsorbed in the arachnoid granulations
Describe the four types of hydrocephalus
• Communicating hydrocephalus is caused by impaired CSF reabsorption in the arachnoid granulations, obstruction of flow in the subarachnoid space, or (rarely) by excess CSF production.
• Noncommunicating hydrocephalus is caused by obstruction of flow within the ventricular system.
• Normal pressure hydrocephalus is characterized by chronically dilated ventricles, sometimes seen in elderly individuals, presenting with symptom triad: gait difficulties, urinary incontinence, and mental decline (wet, wobbly, wacky) - thought to be form of communicating hydrocephalus with impaired CSF reabsorption at arachnoid villi
• Hydrocephalus ex vacuo – excessive CSF in region where brain tissue was lost due to stroke, surgery, trauma, etc. brain loss -> increased CSF -> ventricular enlargement (but normal pressure)
What is Parinaud’s syndrome?
Where third ventricle pushes down into midbrain; result in limited vertical gaze, especially in the upward direction. Particularly in children with acute hydrocephalus, the ominous “setting sun” sign, consisting of bilateral deviation of the eyes downward and inward, may be seen. These abnormalities often reverse after treatment.
Primary CNS vs. metastatic tumors
Primary CNS tumors – arise from abnormal proliferation of nervous system cells
Metastatic tumors – arise from neoplasm (abnormal growth of cells) elsewhere in the body that spread to the brain
Tentorium
Dura fold that separates the occipital and temporal lobes from cerebellum
Supratentorial
Portion of intracranial cavity above the tentorium (e.g., cerebrum)
Infratentorial
Portion of intracranial cavity below the tentorium (e.g., cerebellum)
Meninges
Skull
(Epidural space)
Dura mater (DURAble)
Arachnoid mater (granulations for CSF reabsorption)
Subarachnoid space (blood vessels) (CSF filled)
Pia mater
(Brain)
“PAD”
CN 1
Olfactory
Fx: sensory (smell - the only uncrossed sense)
olfactory loss = anosmia; due to tumor or trauma to orbitofrontal region, viral infections
May result in CSF leakage into nasal cavity
Connects to: frontal lobe
CN 2
Optic
Fx: sensory (vision)
prechiasmic lesion: monocular (one-eye) blindness
postchiasmic lesion: “homonymous hemianopsia” = loss of 1/2 of contralateral visual field on same side of both eyes
Connects to: thalamus
CN 3
Ocuolomotor
Fx: motor (eye movement and pupil restriction)
Compression of CN 3 = fixed or dilated pupil (blown pupil)
Significant constriction (pinpoint pupil) can suggest pons involvement or drug overdose (morphine)
Connects to: midbrain
CN 4
Trochlear
Fx: motor (eyes looking down)
Damage from cerebellar tumors or shearing injury from head trauma
Connects to: midbrain
CN 5
Trigeminal
Fx: motor and sensory (sensory innervation to face muscles, controls mastication)
Connects to: pons
CN 6
Abducens
Fx: motor (outward gaze - damage from increased intracranial pressure)
Connects to: pons
CN 7
Facial
Fx: sensory and motor (controls muscles of facial expressions, taste, and tears/salvation)
Upper motor neuron involvement: facial drooping with forehead
Lower motor neuron involvement: asymmetry of spontaneous facial expressions
Connects to: pons
CN 8
Vestibulocochlear
Fx: sensory (vertigo w/ nystagmus (uncontrolled eye movements) suggests nerve involvement
Connects to: pons
CN 9
Glossopharyngeal
Fx: sensory and motor (touch, pain, and temperature)
gag reflex, same as CN 10
Connects to: medulla
CN 10
Vagus
Fx: (sensory and motor) gag reflex and swallowing
Connects to: medulla
Assess: say “Ah”
CN 11
Spinal accessory
Fx: motor (trapezius muscles/shrugging)
Dysfunction - asymmetrical shrug
Connects to: spinal cord
Sternocleidomastoid strength and trapezius muscle lift are innervated by the ipsilateral cranial nerve XI.
CN 12
Hypoglossal
Fx: motor (tongue muscles)
Lesions: tongue weakness, subtle dysarthria (tongue deviates towards side of lesion) - asked to repeat “Methodist Episcopal”
Connects to: medulla
CN originating sites
olfactory - frontal lobe
optic - thalamus
oculomotor - midbrain
trochlear - midbrain
trigeminal - pons
abducens - pons
facial - pons
vestibulocochlear - pons
glossopharyngeal - medulla
vagus - medulla
spinal accessory - spinal cord
hypoglossal - medulla
Upper vs lower motor neuron
Upper (regulates lower motor neuron):
neuron located within brain/brainstem
body of neuron located in primary motor cortex
axon travels down spinal cord and innervates motor neuron in ventral horn
Lesion (“UPper” “hyper”) - increased tone, muscle reflex, and muscle contraction (spasticity)
can lead to atrophy because of disuse of muscle (b/c limited control)
Babinski sign - toes point up and fan out = upper motor neuron dysfunction in adult
Lower (innervates muscle):
originate in spinal cord
innervates skeletal muscle for movement
Lesion (“hypo” “down”) - decreased muscle tone, muscle reflex, and flaccidity b/c lose inability to control muscle
involuntary muscle contraction
Homunculus of primary motor and sensory cortices
Upper extremity: (medial to lateral) - trunk, arm, hand, face
Lower extremity: in the inter hemispheric fissure
(superior to inferior) - leg, foot
Origination of CN
CN 1 - frontal lobe
CN 2 - thalamus
CN 3-4 - midbrain
CN 5-8 - pons
CN 9-10 and 12 - medulla
CN 11 - spinal cord
Reticular formation
Fx: consciousness and autonomic functions
Neurologic exam
- Consciousness (d/t damage of reticular formation, thalamus (unilateral damage = mild impairment), or cerebral hemispheres
- Orientation
- Memory (poor imm. memory = attention; poor recall = implicate limbic structures/medial temporal lobes)
- Langauge
- Gerstmann’s syndrome (acalculia, agraphia, R/L confusion, finger agnosia) - suggests left parietal lobe
- Apraxia - inability to follow motor commands not due to motor or language deficit
- Neglect - hemineglect most common in R parietal lobe lesion
- Olfaction - CN 1
- Vision and pupillary responses - CN 2 & 3
- Extraocular movement - CN 3, 4, & 6 (smooth pursuit, convergence, saccades, nystagmus)
- Motor exam - lower (damage = decreased tone/spasticity, hypoflexia) and upper (damage = increased tone/spasticity, hyperflexia) motor neurons
…& ataxia - abnormal movements in coordination (cerebellar involvement)
Extraoccular movements
CN 6 (abducens) - lateral rectus muscle, moves eyes laterally
CN 4 (trochlear) - superior oblique muscle, moves eyes down and rotate internally
CN 3 (oculomotor) - all other muscles of eye movement, raises eye lid, and mediates pupillary constriction
Damage to these CN - patients report seeing double vision
Pituitary vs. pineal gland
Pituitary gland - endocrine function, hormones for growth and development -
Press on optic chiasm
Pineal gland - melatonin production and circadian cycle regulation
tumor may obstruct cerebral aqueduct causing hydrocephalus or compress dorsal midbrain causing Parinaud’s syndrome
Glial cell (a.k.a. neuroglia)
Cell in white matter that provides structural support
Ex: Schwann, oligodendrocyte, microglia, ependymal, astrocyte
Brainstem structures
Brainstem = midbrain, pons, medulla
Motor and sensory tracts decussate below medulla and above spinal cord
Tegmentum vs Tectum
Tectum - dorsal (“ceiling”) part of the midbrain; consists of superior colliculi (receives input from retina and visual cortex, fx: tracking objects) and inferior colliculi (receives crossed and uncrossed auditory fibers)
- Posterior to cerebral aqueduct
Tegmentum - ventral (“floor”) part of the midbrain (origin of mesolimbic and mesocortical dopamine pathways)
Anterior to cerebral aqueduct
The cerebral aqueduct separates the tectum and tegmentum
Auditory pathway
Cochlea
Cochlear nucleus (medulla)
Superior olivary complex (pons)
Lateral lemniscus (pons) – area of partial decussation
Inferior colliculus (midbrain)
Medial geniculate nucleus (thalamus)
Auditory cortex (tonotopical)
Visual pathway
1 - Retina rods (periphery of retina, low levels of light and motion) and cones (center of your retina, distinguish color and detail)
2 - Optic nerve
3 - Optic chiasm (area of partial decussation) - becomes optic tract
(wraps around lateral surface of midbrain)
4 - Superior colliculus
5 - Lateral geniculate nucleus (thalamus)
6 - Optic radiations
a - inferior fibers (Meyer’s loop) pass through the temporal lobe; insult = pie in the sky
b - superior fibers of the optic radiations pass through the parietal lobe; insult = pie on the floor
7 - Visual cortex/calcarine fissure (retinotopical) – Brodmann area 17
Optic chiasm lesions produce
Bitemporal hemianopia (generally asymmetrical)
Optic chiasm lies on the ventral surface of the brain, therefore susceptible to compression by pituitary tumors