Neurology Flashcards
Neural development
The notochord induces overlying ectoderm to differentiate into neuroectoderm and form neural plate around day 18. Neural plate gives rise to neural tube and neural crest cells around day 21. Notochord becomes nucleus pulposus of intervertebral disc in adults. The alar plate is dorsal in responsible for sensory. Basal plate is ventral and is responsible for motor.
The three primary vesicles of the developing brain
Prosencephalon (forebrain), mesencephalon (midbrain), rhombencephalon (hindbrain).
Prosencephalon
The forebrain. It differentiates into telencephalon and diencephalon.
Mesencephalon
The midbrain. It differentiates into the secondary mesencephalon.
Rhombencephalon
The hindbrain. It differentiates into the metencephalon and the myelencephalon.
Telencephalon
Derived from the prosencephalon. It differentiates into the cerebral hemispheres and the lateral ventricles.
Diencephalon
It is derived from the prosencephalon. It differentiates into the thalamus and the third ventricle.
Mesencephalon
It differentiates into the midbrain and the aqueduct.
Metencephalon
It is derived from the rhombencephalon. It differentiates into the pons and cerebellum and the upper part of fourth ventricle.
Myelencephalon
It is derived from the rhombencephalon. It differentiates into the medulla and the lower part of the fourth ventricle.
Derivatives of neuroectoderm
It differentiates into CNS neurons, ependymal cells (inner lining of ventricles, make CSF), oligodendroglia, astrocytes.
Derivatives of neural crest
PNS neurons, Schwann cells
Mesoderm
Microglia (like Macrophages, originate from Mesoderm).
Neural tube defects
If neuropores fail to fuse (during the fourth week), than there is a persistent connection between amniotic cavity and the spinal canal. It is associated with low folic acid intake before conception and during pregnancy. There will be an increase in alpha fetoprotein (AFP) in amniotic fluid and maternal serum. Acetylcholinesterase increases in amniotic fluid (fetal AChE in CSF transudates across defect into amniotic fluid). Defects include spina bifida occulta, meningocele, meningomyelocele, and anencephaly.
Spina bifida occulta
There is failure of bony spinal canal to close, but no structural herniation. It is usually seen at lower vertebral levels. The dura is still intact. It is associated with a tuft of hair or dimple at the level of the bony defect. There will be normal AFP. It is the most common neural tube defect.
Meningocele
Meninges (but no neural tissue) herniate through bony defect
Meningomyelocele
Meninges and neural tissue herniate through bony defect.
Anencephaly
A malformation of the anterior resulting in no forebrain and an open calvarium. Clinical findings include an increase in AFP, polyhydramnios (due to no swallowing center in the brain). It is associated with maternal type 1 diabetes. Maternal folate supplementation decreases risk.
Holoprosencephaly
A failure of left and right hemispheres to separate. It usually occurs during weeks 5-6. It may be related to mutations in sonic hedgehog signaling pathway. A moderate form has a cleft lip/palate; the more severe form results in cyclopia. It is seen Patau syndrome and fetal alcohol syndrome.
Chiari I malformation
Cerebellar tonsillar ectopia greater than 3-5 mm. Results in syringomyelia. It is congenital, usually asymptomatic in childhood and manifests with headaches and cerebellar symptoms.
Chiari II malformation
A significant herniation of cerebellar tonsils and vermis through foramen magnum with aqueductal stenosis and hydrocephalus. It often presents with lumbosacral meningomyelocele and paralysis below the defect.
Dandy Walker malformation
Agenesis of the cerebellar vermis with cystic enlargement of the 4th ventricle, which fills the enlarged posterior fossa. It is associated with hydrocephalus and spina
Syringomyelia
A cystic cavity (syrinx) within the spinal cord. If it occurs within the central canal than it can lead to hydromyelia (abnormal widening of the central canal). The crossing anterior spinal commussural fibers are usually damaged first, which results in a cape like, bilateral loss of pain and temperature sensation in the upper extremities (fine touch sensation is preserved). It is associated with Chiari malformations, trauma, and tumors. Syrinx= tube, as in a syringe. It is most common at C8-T1. MRI will show low lying cerebellar tonsils (Chiari I) and fluid filled cavity in spinal cord (syrinx).
Tongue development
The 1st and 2nd brachial arches form the anterior 2/3 (thus sensation via CN V3 and taste via CN VII). the 3rd and 4th branchial arches form the posterior 1/3 (thus sensation and tasted mainly via CN IX, extreme posterior via CN X).
CN responsible for taste
Anterior 2/3 of tongue is CN VII, posterior 1/3 of tongue is CN IX, extreme posterior is CN X.
CN responsible for pain in the tongue
Anterior 2/3 of tongue is CN V3, posterior 1/3 of tongue is CN IX, extreme posterior is CN X.
CN responsible for motor in the tongue
Motor innervation is via CN XII to hyoglossus (retracts and depresses tongue), genioglossus (protrudes tongue), and styloglossus (draws sides of tongue upwards to create a trough for swallowing). Motor innervation is via CN X to palatoglosus (elevates tongue during swallowing).
Nissle stain
Stains cell bodies and dendrites of neurons by staining RER. RER is not present in axons.
Wallerian degeneration
Occurs due to injury of an axon. There is degeneration distal to the injury and axonal retraction proximally. There can be regeneration of axon if it is in the PNS.
Astrocytes
Responsible for physical support, repair, K metabolism, removal of excess neurotransmitter, component of blood-brain barrier, glycogen fuel reserve buffer. Undergoes reactive gliosis (reactive change of glial cells in response to damage). Astrocyte marker in GFAP. It is derived from neuroectoderm.
Microglia
Phagocytic scavenger cells of CNS (mesodermal, mononuclear origin). It is activated in response to tissue damage. It is not readily discernible by a Nissl stain. HIV-infected microglia fuse to form multinucleated giant cells in the CNS.
Myelin
It increases conduction velocity of signals transmitted down axons causing saltatory conduction action potential at the nodes of Ranvier, where there are high concentrations of Ca channels. In CNS, oligodendrocytes myelinate. In PNS, Schwanna cells myelinate. They wrap and insulate axons, increase space constant and increasing conduction velocity.
Schwann cells
Each cell myelinates only 1 PNS axon. Also promote axonal regeneration. Derived from neural crest cells. It increases conduction at nodes of Ranvier, where there is a high concentration of Na channels. They may be injured in Guillain Barre syndrome.
Acoustic neuroma
Occurs in a type of schwannoma. It typically is located in the internal acoustic meatus (CN VII). If bilateral, it is strongly associated with neurofibromatosis type 2.
Oligodendroglia
Myelinates axons of neurons in CNS. Each one can myelinate many axons (around 30). It is the predominant type of glial cell in white matter. It is derived from neuroectroderm. It has a fried egg appearance on histology. It is injured in multiple sclerosis, progressive multifocal leukoencephalopathy (PML), and leukodystrophies.
C nerve fibers
Unmyelinated fibers, slow. In skin, epidermis, and some viscera. It senses pain and temperature.
A-gamma nerve fibers
Myelinated fibers, fast. In skin, epidermis, and some viscera. It senses pain and temperature.
Meissner corpuscles
Large, myelinated fibers; adapt quickly. They are present in glabrous (hairless) skin. It senses dynamic, fine/light touch, position sense.
Pacinian corpuscles
They are large, myelinated, and adapt quickly. They are located in the deep skin layers, ligaments, and joints. It senses vibration and pressure.
Merkel discs
Large, myelinated, adapt slowly. It is located in finger tips and superficial skin. It senses pressure, deep static touch (eg shapes, edges), position sense.
Ruffini corpuscles
Dendritic endings with capsule, adapt slowly. It is located in finger tips and joints. They sense pressure, slippage of objects along surface of skin, and joint angle change.
Endoneurium
invests single nerve fiber layers (inflammatory infiltrate in Guillain- Barre syndrome)
Perineurium
Permible barrier. Surrounds a fascicle of nerve fibers. Must be rejoined in microsurgery for limb reattachment.
Epineurium
Dense connective tissue that surrounds entire nerve (fascicles and blood vessels).
norepinephrine
It increases with anxiety and decreases in depression. It is synthesized in the locus ceruleus (responsible for stress and panic) in the pons.
Dopamine
It increases in Huntington disease and decreases in Parkinson disease and depression. It is synthesized in the ventral tegmentum and substantia nigra pars compacta (midbrain)
5-HT
It decreases in anxiety and depression. It is synthesized in the raphe nuclei in the pons, medulla, and midbrain.
ACh
It increases in Parkinson disease and decreases in Alzheimer and Huntington disease. It is synthesized in the basal nucleus of Meynert.
GABA
It decreases in anxiety and Huntington disease. It is synthesized in the nucleus accumbens (the nucleus accumbens and septal nucleus is the reward center, pleasure, addiction, and fear).
Blood brain barrier
Prevents circulating blood substances (eg bacteria or drugs) from reaching the CSF/CNS. Formed by three structures including tight junctions between non-fenestrated capillary endothelial cells, basement membrane, and astrocyte foot processes. Glucose and amino acids crass slowly by carrier mediated transport mechanisms. Nonpolar/lipid-soluble substances cross rapidly via diffusion. A few specialized regions with fenestrated capillaries and no blood brain barrier allows molecules in the blood to affect brain function (eg area protrema-vomitting after chemo; organum vasculosum of the lamina terminalis (OVLT)- osmotic sensing) or neurosecretory products to enter circulation (eg neurohypophysis-ADH release). Infarction and/or neoplasm destroy endothelial cell tight junctions leads to vasogenic edema. Other notable barriers are the blood testis barrier and maternal fetal blood barrier of placenta.
hypothalamus
The hypothalamus wears TAN HATS: Thirst and water balance, Adenohypophysis control (regulates anterior pituitary), Neurohypophysis releases hormones produced in the hypothalamus, Hunger, Autonomic regulation, Temperature regulation, Sexual urges. Inputs (areas not protected by the blood brain barrier) includes OVLT (organum vasculosum of the lamina terminalis-senses changes in osmolarity), area postrema (responds to emetics). Paraventricular nucleus primarily makes oxytocin. ADH and oxytocin is made by the hypothalamus but is stored and released in the posterior pituitary.
Supraoptic nucleus
Apart of the hypothalamus. Supraoptic nucleus primarily makes ADH.
Paraventricular nucleus
Apart of the hypothalamus. Paraventricular nucleus primarily makes oxytocin.
organum vasculosum of the lamina terminalis
Apart of the hypothalamus, senses changes in osmolarity
area postrema
Apart of the hypothalamus, responds to emetics
Lateral area of the hypothalamus
Controls hunger. Destruction causes anorexia, failure to thrive in infants. It is inhibited by leptin. If you zap the lateral nucleus, you shrink laterally.
Vertomedial area of the hypothalamus
Control satiety. Destruction (eg craniopharyngioma) leads to hyperphagia. It is stimulated by leptin. If you zap your ventromedial nucleus, you grow ventrally and medially.
Anterior hypothalamus
Controls cooling, under parasympathetic control. Anterior nucleus= cool off (cooling, pArasympathetic). A/C=anterior cooling.
Posterior hypothalamus
Controls heating, under sympathetic control. Posterior nucleus= get fired up (heating, sympathetic). If you zap your posterior hypothalamus, you become a Poikilotherm (cold blooded, like a snake).
Suprachiasmatic nucleus
Controls circadian rhythm. You need to sleep to be charismatic (chiasmatic).
Sleep physiology
Sleep cycles are regulated by the circadian rhythm, which is driven by suprachiasmatic nucleus (SCN) of the sypothalamus. Circadian rhythm controls nocternal release of ACTH, prolactin, melatonin, norepinephrine. The activated SCN releases norepinephrine, which acts on the pineal gland to secrete melatonin. SCN is regulated by the environment (eg light). There are two stages: rapid eye movement (REM) and non-REM. Extreaocular movements during REM sleep due to activity of PPRF (paramedian pontine reticular formation/conjugate gaze center). REM sleep occurs every 90 minutes, and duration increases through the night. Alcohol, benzodiazepines, and barbiturates are associated with a decrease in REM sleep and delta wave sleep; norepinephrine also decreases REM sleep.
Treating bedwetting
Treat bedwetting (sleep enuresis) with oral desmopressin (ADH analog). It is prefered over imipramine because of adverse side effects.
Treating night terrors and sleepwalking
Benzodiazepines.
Beta EEG waves
Highest frequency, lowest amplitude. It is active during being awake with eyes open and alert with active mental concentration.
Alpha EEG waves
Active with being awake and eyes closed
Theta EEG waves
Active during stage N1 (5%), which is light sleep.
Sleep spindles and K complexes
Active during stage N2 (45%), which is deeper sleep when bruxism (nocturnal tooth grinding) occurs.
Delta EEG waves
The lowest frequency and highest amplitude. Active during stage N3 (25%). It is the deepest non-REM sleep (slow-wave sleep). This is when sleepwalking, night terrors, and bedwetting occurs.
REM sleep
Occurs 25% of the time. There are beta waves. There is a loss of motor tone, increase brain O2 use, increases and variable pulse and blood pressure. This is when dreaming and penile/clitoral tumescence may occur. It may serve for memory processing function.
EEG wave form order (from wakefulness to REM)
Beta, Alpha, Theta, Sleep spindles and K complexes, Delta, and Beta. At nigh, BATS Drink Blood.
Thalamus
major relay for all ascending sensory information except for olfaction.
Ventral posterolateral nucleus (VPL)
Apart of the thalamus. Receives input from the spinothalamic (pain and temperature) and dorsal columns/medial lemniscus (touch, pressure, vibration and proprioception. It relays info to the primary somatosensory cortex.
Ventral posteromedial nucleus (VPM)
Apart of the thalamus. Receives input from the trigeminal (face sensation) and gustatory (taste) pathway. It relays info to the primary somatosensory cortex. Makeup goes on the face (vpM)
Lateral geniculate nucleus (LGN)
Apart of the thalamus. Receives input from CN II (vision) and relays info to the calcarine sulcus (the primary visual cortex in the frontal cortex). (Lateral=Light).
Medial geniculate nucleus (MGN)
Apart of the thalamus. Receives input from the superior olive and inferior colliculus of tectum (hearing) and relays info to the auditory cortex of the temporal lobe. Medial=Music
Ventral lateral nucleus
Apart of the thalamus. Receives input from the basal ganglia and cerebellum (motor) and relays info to the motor cortex.
Limbic system
A collection of neural structures involved in emotion, long-term memory, olfaction, behavior modulation, ANS function. Structures include hippocampus, amygdala, fornix, mammillary bodies, cingulate gyrus. It is responsible for Feeding, Fleeing, Fighting, Feeling, and Sex. The famous 5 F’S.
Osmotic demyelination syndrome (central pontine myelinolysis)
Acute paralysis, dysarthria, dysphagia, diplopia, loss of consciousness. It can cause locked in syndrome. A massive demyelination in pontine white matter secondary to osmotic changes. It is commonly iatrogenic, caused by overly rapid correction of hyponatremia. In contrast, correcting hypernatremia too quickly results in cerebral edema/ herniation. Correcting serum too fast from low to high, your pons will die; from high to low, your brain will blow.
Cerebellum
It modulates movement; aids in coordination and balance.
Inputs into cerebellum
Inputs include contralateral cortex via middle cerebellar peduncle. Ipsilateral proprioceptive information via inferior cerebellar peduncle from spinal cord.
Outputs from cerebellum
Sends information to contralateral cortex to modulate movement. Output nerves are Perkinje cells, which synapse on the deep nuclei of the cerebellum, which synapses on the contralateral cortex via the superior cerebellar peduncle. The deep nuclei, from lateral to medial, the four deep cerebellar nuclei are the dentate, emboliform, globose, and fastigii. Don’t Eat Greasy Foods.
Lateral lesions of the cerebellum
This part is responsible for voluntary movement of extremities. When injured, propensity to fall toward injured (ipsilateral) side.
Medial lesions of the cerebellum
Lesions involving the midline structures (vermal cortex, fastigial nuclei) and/or flocculonodular lobe causes truncal ataxia (wide-based cerebellar gait), nystagmus, head tilting. Generally, midline lesions result in bilateral motor deficits affecting axial and proximal limb musculature.
Basal ganglia
Important in voluntary movements and making postural adjustments. It receives cortical input and provides negative feedback to cortex to modulate movement.
Striatum
Putamen (motor) and caudate (cognitive)
Lentiform
Putamen and globus pallidus.
D1-Receptor
Dopamine binds to D1, stimulating the excitatory pathway, which facilitates movement.
D2-Receptor
Dopamine binds to D2, inhibiting the inhibitory pathway, which inhibits movement.
Excitatory pathway of the basal ganglia
The cortical inputs stimulate the striatum (putamen), stimulating the release of GABA, which disinhibits the thalamus via the globus pallidus internus/substantia nigra pars reticulata, increasing motion.
Inhibitory pathway of the basal ganglia
The cortical inputs stimulate the striatum (putamen), which disinhibits the subthalamic nucleus via the globus pallidus externus. The subthalamic nucleus stimulates the globus pallidus internus/substantia nigra pars reticulata to inhibit the thalamus, decreasing the motion.
Athetosis
Slow, writhing movements; especially seen in fingers. It is writhing, snake-like movement. The lesion is located in the basal ganglia (eg Huntington).
Chorea
Sudden jerky, purposeless movement. Chorea=dancing. The lesion is located in the basal ganglia (eg Huntington).
Dystonia
Sustained, involuntary muscle contraction. Examples include writer’s cramp; blepharospasm (sustained eye twitch).
Essential tremor
High-frequency tremor with sustained posture (eg outstretched arms), worsened with movement or when anxious. It is often familial. Patients often self-medicate with EtOH, which decreases the tremor’s amplitude. Treatment includes beta-blockers and primidone (a barbiturate).
Hemiballismus
Sudden, wild flailing of 1 arm, with or without the ipsilateral leg. It occurs due to a contralateral lesion in the subthalamic nucleus (eg lacunar stroke). “Half-of-body ballistic.”
Intention tremor
Slow, zigzag motion when pointing/extending toward a target. It is characteristic of cerebellar dysfunction.
Myoclonus
Sudden, brief, uncontrolled muscle contraction. It can present as jerks or hiccups (common in metabolic abnormalities such as renal and liver failure).
Resting tremor
Uncontrolled movement of distal appendages (most noticeable in hands). The tremor is alleviated by intentional movement. For example, pill-rolling tremor of Parkinson disease.
Parkinson disease
Degenerative disorder of CNS associated with Lewy bodies (composed of alpha-synuclein intracellular eosinophilic inclusions) and loss of dopaminergic neurons (ie depigmentation) of substantia nigra pars compacta. Parkinson TRAPS your body: Tremor (pill-rolling tremor at rest), Rigidity (cogwheel), Akinesia (or bradykinesia), Postural instability, Shuffling gait.
Huntington disease
Autosomal dominant trinucleotide repeat disorder on chromosome 4. Symptoms manifest between ages 20 and 50. It is characterized by choreiform movements, aggression, depression, and dementia (sometimes initially mistaken for substance abuse). There is an increase in dopamine and a decrease in GABA and ACh in the brain. Neuronal death occurs via NMDA-R binding and glutamate toxicity. Atrophy of the caudate nucleus with ex vaco dilation of frontal horns on MRI. There is expansion of CAG repeats (anticipation). CAG: Caudate loses ACh and GABA
Broca aphasia
The posterior part of the inferior frontal gyrus of the frontal lobe on the dominant side. Responsible for motor speech. Damage here causes nonfluent aphasia with intact comprehension and impaired repetition. Broca= broken boca. Damage often extends into the primary motor cortex and can be associated with contralateral facial or arm weakness. Patients are aware of deficit and are inevitably frustrated because of lack of ability to express themselves.
Dysarthria vs aphasia
motor inability to speak, a movement deficit. Meanwhile, aphasia is a higher order inability to speak, a language deficit.
Wernicke aphasia
Wernicke (sensory) aphasia occurs from damage to posterior part of the superior temporal gyrus on the dominant side leading to receptive, fluent aphasia (meaning the patient cannot understand any form of language but is able to verbalize fluently, except the speech lacks any meaning). Wernicke is Wordy but makes no sense (what?). In contrast to Broca aphasia, Wernicke aphasia patients are unaware of deficit and show no distress.
Conduction aphasia
Conduction aphasia results from damage to the arcuate fasciculus (connection between Wernicke’s and Broca’s areas). This results in the patient’s inability to repeat words back to someone but an intact ability to comprehend with fluent speech. For example, can’t repeat “no ifs, ands, or buts.”
Global aphasia
Global aphasia results from damage to Broca’s area, Wernicke’s area, and the arcuate fasciculus. This results in a patient with poor comprehension, nonfluent speech, and poor repetition.
Transcortical motor aphasia
Transcortical motor aphasia occurs from damage near Broca’s area producing a nonfluent aphasia where patients are able to comprehend and repeat words after the examiner.
Transcortical sensory aphasia
Transcortical sensory aphasia occurs from damage near Wernicke’s area producing an aphasia where patient are able to speak fluently and repeat words after the examiner, but with poor comprehension.
Mixed transcortical aphasia
Mixed transcortical aphasia is caused by damage to both Wernicke’s area and Broca’s area, but without damage to the arcuate fasciculus. The patient will have nonfluent speech and poor comprehension, but intact repetition.
Kluver-Bucy syndrome
It is characterized by disinhibited behavior (eg hyperphagia, hypersexuality, hyperorality). It occurs due to bilateral lesion of the amygdala. It is associated with HSV-1.
Frontal lobe lesion
Causes disinhibition and deficits in concentration, orientation, judgment. There may be reemergence of primitive reflexes.
Nondominant parietal-temporal cortex lesion
Causes hemispatial neglect syndrome (agnosia [inability to interpret sensations and hence to recognize things] of contralateral side of the world).
Dominant parietal-temporal cortex lesion
Causes Gerstmenn syndrome, which is marked by agraphia (loss in the ability to communicate through writing), acalculia (the inability to do simple mathematics problems), finger agnosia, left-right disorientation.
Reticular activating system lesion
Located in the midbrain. Causes reduced levels of arousal and wakefulness (eg coma).
Wernicke-Korsakoff syndrome
Bilateral lesion of mammillary bodies. Causes confusion, ophthalmoplegia, ataxia; memory loss (anterograde and retrograde amnesia), confabulation, personality changes. It is associated with thiamine (B1) deficiency and excessive EtOH use. It can be precipitated by giving glucose without B1 to a B1-deficient patient.
Basal ganglia lesion
May result in tremor at rest, chorea, and athetosis. Examples include Parkinson and Huntington disease.
Cerebellar hemisphere lesion
Causes intention tremor, limb ataxia, loss of balance. Damage to cerebellum causes ipsilateral deficits, falling toward side of lesion. Cerebellar hemispheres that are laterally located affect lateral limbs.
Cerebellar vermis lesion
Causes truncal ataxia and dysarthria. The vermis is centrally located, affects the central body.
Subthalamic nucleus lesion
Causes contralateral hemiballismus.
Hippocampus (bilateral) lesion
Anterograde amnesia, inability to make new memories.
Paramedian pontine reticular formation lesion
It is located anterior and lateral to the medial longitudinal fasciculus. Causes eyes to look away from side of lesion.
Frontal eye fields lesion
It is located in the frontal cortex. Causes eyes to look towards the lesion.
Anterior cerebral artery distribution
Supplies the anteromedial surface
Middle cerebral artery distribution
Supplies the lateral surface
Posterior cerebral artery
Supplies the posterior and inferior surface.
Watershed zones of the brain
Located between the anterior cerebral and middle cerebral; posterior cerebral and middle cerebral arteries. Damage in severe hypotension, causing upper leg and upper arm weakness, defects in higher order visual processing.
Homunculus
Topographic representation of motor and sensory areas in the cerebral cortex. Feet medially and face laterally.
Regulation of cerebral perfusion
Brain perfusion relies on tight autoregulation. Cerebral perfusion is primarily driven by PCO2 (PCO2 also modulates perfusion in severe hypoxia). Therapeutic hyperventilation (decreases PCO2) helps decrease intracranial pressure (ICP) in cases of acute cerebral edema (stroke, trauma) via vasoconstriction. It is the cause of fainting in panic attacks, due to a decrease perfusion.
Cerebral perfusion and blood pressure
Cerebral perfusion relies on a pressure gradient between mean arterial pressure (MAP) and ICP. A decrease in blood pressure or an increase in ICP causes a decrease in cerebral perfusion pressure (CPP). CPP=MAP-ICP. If CPP=0, there is no cerebral perfusion, which causes brain death.
Middle cerebral artery
Supplies the motor cortex (upper limb and face), lesions here cause contralateral paralysis of the upper limb and face. Also supplies sensory cortex (upper limb and face), lesion causes contralateral loss of sensation of the upper limb and face. Also supplies temporal lobe (Wenicke area) and frontal lobe (Broca area). A lesion here can cause aphasia if in dominant (usually left) hemisphere. Hemineglect if lesion is on the non dominant side (usually right).
Anterior cerebral artery
Supplies the motor cortex (lower limbs). A lesion here would cause contralateral paralysis. It also supplies the sensory cortex (lower limb) and a lesion here would cause loss of sensation on the contralateral lower limb.
Lenticulostriate artery
Supplies the stratum and internal capsule. A lesion would cause contralateral hemiparesis and hemiplegia. This is a common location of lacunar infarcts, secondary to unmanged hypertension.
Anterior spinal artery
Supplies the lateral corticospinal tract (carries motor), a lesion here causes contralateral hemiparesis of both the upper and lower limbs. It also supplies the medial lemniscus (carries vibratory and touch-pressure sense); a lesion here causes a decrease in contralateral proprioception. Strokes here are commonly bilateral.
Medial medullary syndrome
Stroke in the paramedian branches of the anterior spinal artery or vertebral arteries can produce a medial medullary syndrome, which presents with: Contralateral hemiparesis of the upper and lower limbs (lesion of lateral corticospinal tract); Contralateral decreased proprioception, vibration sense, and discriminative touch (lesion of medial lemniscus); Ipsilateral hypoglossal dysfunction with the tongue deviating to the ipsilateral side (lesion of caudal medulla)
Posterior inferior cerebellar artery
Supplies the lateral medulla, including the vestibular nuclei (vomiting, vertigo, nystagmus), lateral spinothalamic tract, spinal trigeminal nucleus (a decrease in pain and temperature sensation from ipsilateral face and contralateral body), nucleus ambiguus (dysphagia, hoarseness, decrease gag reflex), sympathetic fivers (ipsilateral horner syndrome), and inferior cerebellar peduncle (ataxia and dysmetria). A lesion here results in lateral medullary (Wallenberg) syndrome. Nucleus ambiguus effects are specific to PICA lesions. Don’t pick a (PICA) horse (hoarseness) that can’t eat (dysphagia).
Anterior inferior cerebellar artery
Supplies the lateral pons, which contain the cranial nerve nuclei, vestibular nuclei (vomiting vertigo, nystagmus), facial nucleus (paralysis of face, decrease of lacrimation, salivation, decrease in taste from anterior 2/3 of tongue), spinal trigeminal nucleus (ipsilateral decrease in pain and temperature of the face, contralateral decrease in pain and temperature of the body), cochlear nuclei, and sympathetic fibers. It also supplies the middle and inferior cerebellar peduncles (ataxia and dysmetria). Causes lateral pontine syndrome. Facial nucleus effects are specific to AICA lesions. “Facial droop means AICA’s pooped.”
Posterior cerebral artery
Supplies occipital cortex and visual cortex. Lesion here causes contralateral hemianopia (blindness over half the field of vision) with macular sparing.
Basilar artery
Supplies the pons, medulla, lower midbrain, corticospinal and corticobulbar tracts, ocular cranial nerve nuclei, paramedian pontine reticular formation. A lesion here preserves consciousness and blinking, but causes quadriplegia, loss of voluntary facial, mouth, and tongue movements. This is called locked in syndrome.
Anterior communicating artery
The most common lesion here is aneurysm, which can lead to stroke. A saccular (berry) aneurysm can impinge cranial nerves. It usually manifests as visual field defects.
Posterior communicating artery
This is a common site of saccular aneurysm, not strokes. It can result in CN III palsy (eye is down and out with ptosis and mydriasis).
Saccular (berry) aneurysm
Occurs at bifurcations in the circle of Willis. Most common site is junction of anterior communicating artery and anterior cerebral artery. Rupture (the most common complication) causes subarachnoid hemorrhage (the worst headache of my life) or hemorrhagic stroke. It can also cause bitemporal heminopia via compression of the optic chiasm. It is associated with ADPKD, Ehlers-Danlos syndrome. Other risk factors include advanced age, hypertension, smoking, race (increase risk in blacks).
Charcot Bouchard microaneurysm
It is associated with chronic hypertension; affects small vessels (eg basal ganglia or thalamus).
Central post stroke pain syndrome
Neuropathic pain due to thalamic lesions. Initial paresthesias followed in weeks to months by allodynia (ordinarily painless stimuli cause pain) and dysesthesia. It occurs in 10% of stroke patients.
Epidural hematoma
Due to rupture of middle meningeal artery (branch of maxillary artery), often secondary to fracture of temporal bone. There is a lucid interval than rapid expansion under systemic arterial pressure causes transtentorial herniation, CN III palsy. CT shows biconvex (lentiform), hyperdense blood collection that does not cross suture lines. It can cross falx, tentorium.
Subdural hematoma
Rupture of bridging veins causing a slow venous bleeding (less pressure=hematoma develops over time). Seen in elderly individuals, alcoholics, blunt trauma, shaken baby (predisposing factors include brain atrophy, shaking, and whiplash). Crescent shaped hemorrhage that crosses suture lines. Mid line shift. Cannot cross falx, tentorium.
Subarachnoid hemorrhage
Rupture of an aneurysm (such as a berry aneurysm, as seen in Ehlers-Danlos syndrome, ADPKD) or arteriovenous malformation. There is a rapid time course. Patients complain of worst headache of my life. Bloody or yellow (xanthochromic) spinal tap. 2-3 days afterword, there is a risk of vasospasm due to blood breakdown (not visible on CT, treat with nimodipine) and rebleed (visible of CT).
Intraparenchymal hemorrhage
It is most commonly caused by systemic hypertension. It is also seen with amyloid angiopathy (recurrent lobar hemorrhagic stroke in elderly), vasculitis, neoplasm. Typically occurs in basal ganglia and internal capsule (Charcot Bouchard aneurysm of lenticulostriate vessels), but it can be lobar.
Ischemic brain disease, stroke
Irreversible damage begins after 5 minutes of hypoxia. The most vulnerable areas are the hippocampus, neocortix, cerebellum, watershed areas. It causes irreversible neuronal injury. Noncontrast CT to exclude hemorrhage (before tPA can be given). CT detects ischemic changes in 6-24 hours. Diffusion weighted MRI can detect ischemia within 3-30 min. With ischemic hypoxia, hippocampus is most vulnerable.
Histological features of stroke after 12-48 hours
Red neurons
Histological features of stroke after 24-72 hours
Necrosis plus neutrophils
Histological features of stroke after 3-5 days
Macrophages (microglia
Histological features of stroke after 1-2 weeks
Reactive gliosis plus vascular proliferation
Histological features of stroke after over 2 weeks
Glial scar
Hemorrhagic stroke
Intracerebral bleeding often due to hypertension, anticoagulation, cancer (abnormal vessels can bleed). It may be secondary to ischemic stroke followed by reperfusion (increases vessel fragility). Basal ganglia are most common site of intracerebral hemorrhage.
Ischemic stroke
Acute blockage of vessels cause a disruption of blood flow and subsequent ischemia, leads to liquefactive necrosis. There are three types: Thrombotic, embolic and hypoxic.
Thrombotic ischemic stroke
It occurs due to a clot forming directly at the site of infarction (commonly the MCA), usually over an atherosclerotic plaque.
Embolic ischemic stroke
An embolus from another part of the body obstructs vessel. It can affect multiple vascular territories. Examples include atrial fibrillation, DVT with patent foramen ovale.
Hypoxic ischemic stroke
It occurs due to hypoperfusion or hypoxemia. It is common during cardiovascular surgeries. It tends to affect watershed areas.
Treatment of ischemic stroke
tPA if within 3-4.5 hours of onset and no hemorrhage/ risk of hemorrhage. Reduce risk with medical therapy (eg aspirin, clopidogral). Optimum control of blood pressure, blood sugars, lipids. Treat conditions that could increase risk (eg A fib).
Transient ischemic attack
Brief, reversible episode of focal neurologic dysfunction without acute infarction (without MRI), with the majority resolving in under 15 minutes. Deficiets are due to focal ischemia.
Dural venous sinuses
Large venous channels that run through the dura. They drain the blood from cerebral veins and receive CSF from arachnoid granulations. They empty into the internal jugular vain.
Superior sagittal sinus (SSS)
The SSS is a large sinus between the two hemispheres. It is embedded within the falx cerebri and drains to the confluence of sinuses (which also receives blood from the straight sinus). In turn, the confluence empties laterally into the 2 transverse sinuses. A subdural hematoma forms when the cerebral veins draining to the SSS are ruptured during head trauma and appears as “crescent” shaped on imaging.
Transverse sinus
The transverse sinus is the lateral continuation of the confluence of sinuses. It curves inferiorly to become the sigmoid sinus.
Sigmoid sinus
The sigmoid sinus drains to the internal jugular vein.
Cavernous sinus
The cavernous sinus is located just lateral to the body of the sphenoid. Cranial nerves III, IV, V1, V2, VI, as well as the internal carotid artery, must pass through the cavernous sinus en route to their destinations.
Ventricular system
The lateral ventricle drains into the third ventricle via the right and left interventricular foramina of Monro. The third ventricle drains into the fourth ventricle via the cerebral aqueduct of Syvius. The fourth ventricle drains into the subarachnoid space via the foramina of Luscka (lateral) and the foramen of magendie (medial). CSF is made by the ependymal cells of choroid plexus, it is reabsorbed by the arachnoid granulations and then drains into the dural venous sinuses.
Idiopathic intracranial hypertension (pseudotumor cerebri)
An increase in ICP with no apparent cause on imaging (ie hydrocephalus, obstruction of CSF outflow). Patients present with headache, diplopia (usually from CN VI palsy), no mental status alterations. Papilledema seen on exam. risk factors include being a women of childbearing age, vitamin A excess, danazol. Lumbar puncture reveals increase of opening pressure and provides headache relief. Treatment include weight loss, acetazolamide, topiramate, invasive procedures for refractory cases (eg repeat lumbar puncture, CSF shunt placement, optic nerve fenestration surgery).
Communicating hydrocephalus
A decease in CSF absorption by arachnoid granulations cases an increase in ICP, papilledema, herniation (eg arachnoid scarring post-meningitis).
Normal pressure hydrocephalus
Affects the elderly. It is idiopathic. CSF pressure elevated only episodically. It does not result in increased subarachnoid space volume. Expansion of ventricles distorts the fibers of the corona radiata causing a triad of urinary incontinence, ataxia and cognitive dysfunction (sometimes reversible). “Wet, wobbly, and wacky”
Noncommunicating hydrocephalus
Caused by structural blockage of CSF circulation within ventricular system (eg stenosis of aqueduct of Sylvius; colloid cyst blocking foramen Monro).
Ex vacuo ventriculomegaly
Appearance of an increase CSF on imaging, is actually due to decreased brain tissue (neuronal atrophy) (eg Alzheimer disease, advanced HIV, Pick Disease). ICP is normal. Triad (Wet, wobbly, and wacky) is not seen.
Spinal nerves
There are 31 pairs of spinal nerve in total: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal. Nerves C1-C7 exit above the corresponding vertebra. C8 spinal nerves exits below C7 and above T1. All other nerves exit below (eg C3 exits above the 3rd cervical vertebra; L2 exits below the 2nd lumbar vertebra). There are 31, just like 31 flavors of Baskin-Robbins ice cream.
Vertebral disc herniation
The nucleus pulposus (soft central disc) herniates through annulus fibrosus (outer ring), usually occurs posterolaterally at L4-L5 or L5-S1.
Lower extent of spinal cord
In adults, spinal cord extends to lower border of L1-L2 vertebrae. Subarachnoid space (which contains the CSF) extends to lower border of S2 vertebra.
Lumbar puncture
Lumbar puncture is usually performed between L3-L4 or L4-L5 (level of cauda equina). Goal of lumbar puncture is to obtain sample of CSF without damaging spinal cord. To keep the cord alive, keep the spinal needle between L3 and L5.
Spinal cord and associated tracts
Legs (Lumbrosacral) are Lateral in Lateral corticospinal and spinothalamic tracts. Dorsal column is is organized as you are, with hands at sides. Arms outside legs inside.
Dorsal column
Ascending tract carrying info about pressure, vibration, fine touch, and proprioception. Fasciculus gracilis is medial and carries info from lower body and legs. The gasciculus cuneatus is lateral and carries info from upper body and arms. Sensory nerve endings carry info to cell body in dorsal root ganglion, which enters the spinal cord and ascends ipsilaterally in dorsal column. The first synapse is on the ipsilateral nucleus cuneatus or gracilis in the medulla. The second order neuron decussates in medulla and than ascends contralaterally in medial lemniscus. The second synapse occurs in the ventral posterolateral nucleus (VPL) in the thalamus. The 3rd order neuron travels to the sensory cortex.
Spinothalamic tract
Ascending tract. The lateral portion carries info about pain and temperature (the info from the sacral region travels laterally to the info from the cervical region). The anterior portion carries info about crude touch and pressure. Sensory nerve ending (Agamma and C fivers) (cell body in dorsal root ganglion) and enters the spinal cord. The first synapse occurs in the ipsilateral gray matter within the spinal cord. The second order neuron decussates at the anterior white commissure and ascends contralaterally. The second synapse occurs in the ventral posterolateral nucleus (VPL) in the thalamus. The 3rd order neuron travels to the sensory cortex.
Lateral corticospinal tract
A descending tract carrying info for voluntary movement of contralateral limbs. The cell body of the UMN located in the primary motor cortex and descends in ipsilaterally through the internal capsule. Most of the fibers decussate at caudal medulla in the pyramidal decussation and then descends contralaterally. The fibers that crossed (80%) travel in the lateral corticospinal tract with info traveling to sacral region most lateral and the info traveling to the cervical region being most medial. These fibers control movement in the limbs. The fibers that do not cross control the axial of the body and travel in the anterior corticospinal tract. The first synapse occurs on the cell bodies of the LMN in the anterior horn of the spinal cord. The LMN than leaves the spinal cord and synapses on the NMJ.
Signs of UMN lesion
weakness, hyperreflexia, increased tone, babinski sign (after the sole of the foot has been firmly stroked, the big toe then moves upward or toward the top surface of the foot), spastic paralysis, and clasp knife spasticity (a stretch reflex with a rapid decrease in resistance when attempting to flex a joint). Upper MN= everything UP (tone, DTRs, toes).
Signs of LMN lesion
Weakness, atrophy, fasciculations (muscle twitching), decrease reflexes, decrease tone, flaccid paralysis. Lower MN= everything lowered (less muscle mass, decrease muscle tone, decrease reflexes, down going toes).
Spinal lesion in Werdnig-Hoffmann disease
Poliomyelitis and spinal muscular atrophy. It is a LMN lesions due to destruction of the anterior horns and leads to flaccid paralysis.
Spinal lesion in Multiple sclerosis
Occurs due to demyelination. It most commonly effects the white matter of the cervical region. There are random and asymmetric lesions, due to demyelination. Produces scanning speech, intention tremor, and nystagmus.
Spinal lesion in Amyotrophic lateral sclerosis
There are combined UMN and LMN deficits with no sensory or oculomotor deficits. There are both UMN and LMN signs. It can be caused by a defect in superoxide dismutase 1. It commonly presents as fasciculations with eventual atrophy and weakness of hands. It is eventually fatal. Riluzole treatment modestly increases survival by decreasing presynaptic glutamate release. It is commonly known as Lou Gehrig disease. For LOU gehrig disease, give riLOUzole.
Spinal lesion in complete occlusion of the anterior spinal artery
It spares dorsal columns and Lissauer tract. The upper thoracic anterior spinal artery territory is watershed area, as artery of Adamkiewicz supplies ASA below T8.
Spinal lesion in Tabes dorsalis
It is caused tertiary syphilis. It results from degeneration (demyelination) of the dorsal columns and roots causes impaired sensation and proprioception, progressive sensory ataxia (inability to sense or feel the legs causing poor coordination). It is associated with Charcot joints, shooting pain, Argyll Robertson pupils. Exam will demonstrate absence of DTRs and positive Romberg sign (the standing patient is asked to close his or her eyes causing a loss of balance).
Spinal lesion in Syringomyelia
Syrinx expands an damages the anterior commissure of spinothalamic tract (2nd order neurons), which causes bilateral loss of pain and temperature sensation (usually C8-T1). It is seen with Chiari I malformation. It can expand and affect other tracts.
