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74 Cards in this Set
- Front
- Back
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Basal ganglia and thalamus embryology
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Basal ganglia: telencephalic derived from lateral ventricles
Thalamus: diencephalic derived from third ventricle |
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Striatum
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Composed of caudate and putamen
Connected by cellular bridges Pierced by internal capsule (white matter) which pass through cellular bridges Caudate is always next to lateral ventricle |
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Lentiform
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Globus pallidus and putamen
Globus pallidus medial to putamen |
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Thalamus as a relay
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Information to cortex from sensory (except olfaction), basal ganglia, cerebellum, brainstem reticular formation, and limbic system
Cortical input to thalamus to filter the relay of information |
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Subcortical centers
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Basal ganglia and thalamus
Contain large number of neurons for information processing |
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Cortex formation
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"inside out" from lateral ventricles
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Nucleus accumbens
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formed from ventral striatum
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Anterior limb of internal capsule
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Always lies between the putamen and caudate in regions anterior to the thalamus and third ventricle
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Basal forebrain nuclei
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Located underneath anterior commisure
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Posterior limb of internal capsule
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Lies between putamen and thalamus
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Thalamus anatomy general
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Lamina divides into medial, lateral, and anterior groups
Thalamic reticular layer outlines Intralaminar nuclei within dividing lamina |
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Body somatosensory projection to thalamus
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Body to VPL nucleus
-dorsal column to nucleus cuneatus and gracilis, cross, medial lemniscus to VPL -Anterolateral to VPL |
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Face somatosensory projection to thalamus
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Face to VPM nucleus
-vibration synapse in principle sensory nucleus of V, neurons cross in pons and ascend in trigeminal lemniscus -pain in face synapse in spinal nucleus of V, cross and ascend as trigeminal thalamic tract |
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Visual information projection to thalamus
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Visual to LGN (lateral geniculate) nucleus
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Auditory information projection to thalamus
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Audition to MGN (medial geniculate) nucleus
-info from cochlear ganglia synapse in cochlear nuclei to superior olivary complex in pons, to inferior collisculus |
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Thalamic motor loop
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Globus pallidus (to ventral anterior and ventral lateral), cerebellum (to ventral lateral), cortex feed info to thalamus which drives primary motor cortex and motor association cortex
Cortex gives input to striatum, pons (to cerebellum) |
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Limbic thalamic relay
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Project to the medial and anterior groups of thalamic nuclei which then diffuse projections to the prefrontal cortex and cingulate gyrus
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Amygdala and hippocampus
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The Amygdala lies within the uncus and the parahippocampal gyrus. This nuclear complex is important in many emotions and drives.
The Hippocampal formation is an extensive fold of archicortex (“ancient or first cortex”) containing only 3 layers. This region is important for memory function and learning. |
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Ventricle anatomy
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Lateral ventricles
-body and atrium -foramen of monro -anterior, posterior, temporal horn Third ventricle -sometimes massa intermedia passes through Cerebral aqueduct of Sylvius -tectum and tegmentum of midbrain surround Fourth ventricle -roof is cerebellum -CSF escapes in lateral foramina of lushka and inferior foramen of magendie |
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Subarachnoid spaces and cisterns
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cisterna magna
interpeduncular cistern prepontine cistern quadrigeminal cistern ambient cistern |
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CSF release and absorption
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Released by choroid plexus
Reabsorbed by arachnoid villi |
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Nucleus Solitarius
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sensory relay nucleus for special taste (cn VII, IX and X) and visceral sensory data from the carotid sinus, aortic arch and organs in the thorax and abdomen (cn IX and X). All these cranial nerves have their own senosry ganglia containing the cell bodies and the solitary nucleus is a sensory relay nucleus that projects to the thalamus.
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Nucleus Ambiguous
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motor nucleus. It is a collection of motor neurons that innervate skeletal muscle in the pharynx and larynx (cranial nerves IX and X).
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Trigeminal spinal nucleus
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relay nucleus for all pain and temperature fibers for all cranial nerves. The spinal nucleus of the trigeminal is also a relay nucleus for several cranial nerves with pain and temperature fibers, mostly Trigeminal V , but also Facial VII, Glossopharyngeal IX, and Vagus X)
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Levels of CN nuclei in brainstem
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Midbrain: CN 3 & 4
Pons: CN 5, 6, 7, part of 8 Medulla: part of CN 8, CN 9, 10, 11, 12 Special cases: mesencephalic nucleus of 5 extends into midbrain (proprioception of jaw) spinal tract and nucleus of 5 extends from the mid-pons down to C2 (pain and temperature sensation of the face) |
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Blood supply to brain
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1. Posterior Blood Supply:
-Vertebral arteries --anterior spinal artery (middle medulla) --posterior spinal artery --posterior inferior cerebellar artery (dorsolateral medulla) --Basilar artery ---anterior inferior cerebellar artery (dorsolateral pons) ---superior cerebellar artery (dorsal midbrain) ---posterior cerebral artery (lateral midbrain) ----posterior communicating 2. Anterior Blood Supply -Internal carotid arteries --middle cerebral artery --anterior cerebral artery ---anterior communicating |
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CNIII and PCA and SCA
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CNIII exits between PCA and SCA
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CNIII parasympathetic
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Edinger westphal nucleus to CNIII to ciliary ganglia to short ciliary (V1)
Pupil constriction and lens accomodation |
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Extraocular eye muscle neurons
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The SO (superior oblique) is innervated by CN IV
The LR (lateral rectus) is innervated by CN VI AR (all the rest of the extraocular muscles) are innervated by CN III Note that III and VI exit the brain in the midline above and below the pons while IV is the only cranial nerve to exit on the dorsal surface. All three nerves enter the orbit through |
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Reticular formation
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the midbrain, pons and medulla
This is a network of interconnected collections of neurons (nuclei) dispersed alongside long tracts descending and ascending the brainstem. |
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Pons blood supply
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Upper:
Middle - Basilar artery (paramedian) Lateral - Basilar artery (circumferential) Dorsal - SCA Lower: Middle - Basilar (paramedian) Lateral and dorsal - AICA and Basilar (circumferential) |
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Trigeminal overview
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CN V: This system will provide for the head the same sensory information that the medial lemniscus and anterolateral pathway provide for the body.
CN V exits the brainstem at mid-pons and passes within the semi-lunar (trigeminal ) sensory ganglia where it is subdivided into 3 divisions: V1-Opthalmic - Exits Supraorbital Fissure V2-Maxillary - Exits Foramen Rotundum V3-Mandibular - Exits Foramen Ovale 3 Sensory Nuclei: Spinal nucleus of V (a relay for pain and temperature it’s analogous to the anterolateral pathway for the body) Principal (chief or main) sensory nucleus – (a relay for fine touch it’s analogous to the dorsal column medial lemnisucs pathway for the body) Mesencephalic nucleus of V – (a unique nucleus specialized for proprioception of chewing eye and tongue muscles, this is the ONLY case where sensory neurons are found in the CNS and not in a peripheral ganglion). Motor Nucleus The trigeminal also has a motor nucleus for the muscles of mastication (as well as the mylohyoid, ant. Digastric, tensor veli palatini and tensor tympani) |
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CN VII motor
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Note the motor nucleus of VII has a motor root that enters the internal acoustic meatus and bends in the temporal bone (a genu or knee like bend). The motor root of VII exits the stylomastoid foramen. It passes through the parotid gives off 5 branches (like 5 fingers). These 5 branches emerge from the anterior border of the gland to innervate the muscles of facial expression (ten zebras bit my cousin – temporal, zygomatic, buccal mandibular, cervical).
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UMN vs LMN facial paralysis
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a UMN (upper motoneuron) facial lesion (ie. stroke in the right motor cortex) results in paralysis on the opposite side only below the eye. The frontalis muscle moves the skin of the forehead and the obicularis oculi muscle tightly shuts the eye. The motor neurons innervating these muscles receive umn innervation from both sides of the brain while the motor neurons innervating the facial muscles below the eye only receive umn from the opposite side of the brain (so an umn lesion in the right motor cortex would only paralyze the facial muscles on the left side below the eye.
a LMN (lower motoneuron) facial lesion (lesion of the facial motor nucleus or the facial nerve or parotid cancer etc.) can result in the paralysis of all muscles on the same side of the lesion. |
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Medullary blood supply
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Middle - vertebral (paramedian) and anterior spinal
Lateral - Vertebral and PICA |
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Hypoglossal nerve test
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The tongue protrudes normally straight ahead (the balanced symmetry of the actions of both genioglossus muscles on the left and right sides) but a lmn injury to the XII nerve results in a deviation of the protruding tongue toward the lesion – the weak (unopposed) genioglossal muscles and therefore toward the injured XIIth cranial nerve.
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Vagus nerve test
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The uvula points away from the side with weak muscles (vagal injury)
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Cooperative patient interview
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Disorder centered mode
-Interviewer acts in a professional manner and assumes that the patient seeks help voluntarily and will answer all questions. |
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Difficult patient interview
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Patient centered mode
-To obtain a comprehensive diagnosis and to judge the patient’s capacity for staying in treatment, the interviewer explicitly focuses on establishing a cooperative relationship with the patient |
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Advanced rapport strategies
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Comfort
Empathy Insight Show expertise |
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Cognitive assessment, different approaches
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Formal neuropyschological testing
-standardized instruments and methods -comparable norms Bedside testing -screening battery (MMSE) -tailored bedside testing |
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MMSE
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Orientation
-Date -Place Language -naming -repeating -verbal commands -written commands -writing -drawing Attention -serial sevens Memory -register 3 objects -recall 3 objects |
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Astrocytes overview
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Envelop basement membranes of capillaries, neurons, and synapses
Maintain blood brain barrier Involved in metabolism of some neurotransmitters Buffer potassium concentration of extracellular space Proliferate in reaction to injury forming glial scars = gliosis Contain GFAP (glial fibrillary acidic protein) |
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Oligodendroglia overview
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Myelin-forming cells in CNS.
Each oligo can myelinate up to 30-50 axons; each oligo forms one internode of myelin on any given axon. |
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Ependymal cells overview
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Ciliated cells (above right) joined by apical tight junctions and line the ventricles of the brain and central canal of the spinal cord. The choroid plexus (below right), which produces cerebrospinal fluid (CSF), is continuous with, and a derivative of, the ependyma.
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Microglia overview
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Part of the monocyte-macrophage system.
Proliferate as macrophages in reaction injury to phagocytose damaged tissue (upper picture). Also proliferate in viral infections (lower picture). Primary CNS lymphoma arises from this type of cell. |
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Unusual features of CNS
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Localization of function
Autoregulation of blood flow Response to injury -gliosis rather than fibrosis Selective vulnerability -neurons more sensitive to ischemia -different regions more sensitive Unusual anatomical features -enclosed by skull -CSF -NO LYMPHATICS |
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Epidural, subdural, subarachnoid compartments
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Epidural: between skull and dura
Subdural: between inner dura and arachnoid Subarachnoid: between arachnoid and pial surface of brain |
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Lumbar puncture and normal CSF profile
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CSF can be studied by removing it from the subarachnoid space (SAS), usually by doing a lumbar puncture. Recall that the spinal cord in an adult terminates at about the L1-L2 level. Using the iliac crest as an external landmark for the L4 vertebral body, a needle can be inserted into between L4 and L5 into the thecal sac
WBC <10/mm^3 (lymphs only) Protein 15-45 mg/dl glucose 50-100 mg/dl |
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Ommaya reservoir
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Ventricular catheter attached to a subcutaneous reservoir under the scalp. Percutaneous injection facilitates distribution of the drug
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Blood brain barrier
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Brain capillary endothelial cells are jointed by tight junctions, which is different from systemic capillaries. CNS capillaries are also surrounded by astrocyte cell processes, which also contribute to the blood-brain barrier.
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Causes of hydrocephalus
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Overproduction of CSF (rare):
Choroid plexus papilloma Obstruction of CSF flow: Within the ventricular system Outside the ventricular system -In the subarachnoid space, e.g., meningeal fibrosis due to previous meningitis or subarachnoid hemorrhage. -Defective absorption by the arachnoid granulations (very rare) |
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Communicating vs noncommunicating vs ex vacuo hydrocephalus
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Communicating:
An obstruction to CSF flow outside the ventricular system or defective reabsorption of CSF results in dilation of all ventricles. Since all ventricles are patent, they “communicate” with each other. Noncommunicating: Obstruction of flow of CSF within the ventricular system so that the ventricular cavities no longer “communicate” with each other. Ex vacuo: Compensatory dilation of ventricles in response to loss of tissue volume; not accompanied by increased intracranial pressure |
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Cerebral edema
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Vasogenic:
-Due to increased capillary permeability (breakdown of blood-brain barrier) -Plasma filtrate accumulates in extracellular space Cytotoxic: -Increased intracellular sodium and water causes swelling of cells Interstitial: -CSF enters extracellular space of periventricular white matter from the ventricles across the ependyma No lymphatics to drain fluid |
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Monro-Kellie Hypothesis
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Bony calvarium limits intracranial capacity
Normal intracranial contents include: Neural parenchyma (about 1400 ml) Blood (about 75 ml) Cerebrospinal fluid (about 75 ml in cranium) Therefore, an increase in volume of one component can only occur at the expense of the other two. When intracranial pressure increases to a critical level, it will exceed mean arterial blood pressure and cerebral perfusion will cease. This is what occurs in brain death |
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Subfalcial herniation
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herniation can cause compression of the anterior cerebral arteries.
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Transtentorial (uncal) herniation
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, the medial temporal lobe usually compresses the ipsilateral oculomotor nerve, the cerebral peduncle, and sometimes the posterior cerebral artery. Ultimately, the brainstem is compressed which results in death if the pressure is not relieved
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Central herniation
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This form of herniation is usually due to bilateral hemispheric edema. It results in bilateral transtentorial herniation and compression of the midbrain. The pupillary light reflex pathway in the midbrain tectum is affected causing unreactive pupils.
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Duret hemorrhages
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Hemorrhages in brainstem due to compression of vessels during herniation
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Normal intracranial pressure
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<20 cm h20 or <15 mm Hg
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Papilledema
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Intracranial pressure is transmitted along the subarachnoid space (surrounding the optic nerves). Pressure on the nerves interferes with axoplasmic flow and venous return resulting in swelling of the optic disc……recall that the optic nerve is made up of axons of retinal ganglion cells so direction of flow is from the cell bodies in the retina toward the brain.
You should always try to look for papilledema if a patient exhibits signs of increased intracranial pressure. The absence of papilledema does not rule out increased intracranial pressure because is takes hours to days to develop. You should check for papilledema before attempting a lumbar puncture, because increased intracranial pressure is a relative contraindication to performing a lumbar puncture because of the possibility of precipitating herniation. Papilledema causes an increase in the blind spot and can be experienced by patients has loss of vision or blurred vision. |
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Treatment for elevated intracranial pressure
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Elevate head 30 degrees
-promote venous drainage Intubate and hyperventilate to pCO2 of 25-30 mm Hg -cerebral vasoconstriction Serum osmolarity Ventricular drainage Barbituate induced coma Hemicraniectomy Steroids |
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Skull fractures
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Linear: usually temporoparietal, where bone is thinnest
Depressed: fragment(s) displaced inward Comminuted: multiple fragments Open or compound: scalp laceration overlying fracture; risk of infection or CSF leak. Diastatic: fractures that cross suture lines Fractures of subsequent injuries do not cross fracture lines of prior injuries |
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Base of skull fracture clinical signs
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Ears: hemotympanum (blood behind TM), tympanic perforation, CSF otorrhea (CSF leaking from ear), hearing loss
Facial weakness (damage to facial nerves) Ecchymosis over mastoid (Battle sign) CSF rhinorrhea (CSF leaking from nose) Anosmia (loss of sense of smell; here due to damage to olfactory bulbs) Bilateral periorbital ecchymosis (raccoon eyes) |
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Contusions: coup and contrecoup
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Coup (at site of impact)
Contrecoup (on opposite side of head from impact site) -Brain strikes opposite inner surface of skull after sudden deceleration These look the same Need forensic evidence to decide where impact occurred In general, if head is immobile at time of impact, only coup injury is seen. Commonly seen in inferior frontal and anterior temporal areas as brain moves over rough floor of anterior fossa or strikes the sphenoid ridge Focal hemorrhages, usually wedge-shaped with base at cortical surface (on the crests of the gyri), due to scraping or bruising of brain |
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Epidural hematoma
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Usually due to laceration of meningeal artery (esp., middle meningeal artery) and is associated with skull fracture
15% bleed from laceration of one of dural sinuses Arterial blood under pressure strips dura from skull and can accumulate rapidly Usually requires emergent surgical evacuation |
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Subdural hematoma
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Tearing of bridging veins
People with brain atrophy at increased risk (e.g., elderly, alcoholic) Acute SDH is often associated with underlying brain injury Chronic SDH may occur after trivial injury or without (recalled) history of trauma; may rebleed; long-standing hematoma liquifies and is called hygroma Both acute and chronic SDH can cause significant mass effect requiring surgical evacuation |
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Diffuse axonal injury
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Persistent unconsciousness after injury
No other cause of coma identified on imaging Shearing of axons Important cause of persistent disability after traumatic brain injury (TBI) With amyloid-precursor protein (APP) staining (right) swollen axons may be seen about 3 hours after injury. It takes about 18-24 hours to see them on H&E stained sections (left). |
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Concussion symptoms
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Definition: trauma-induced alteration in mental status
-May or may not involve loss of consciousness -Confusion and amnesia are the hallmarks of concussion. -Confusional episode and amnesia may occur immediately after the blow to the head or several minutes later. Early symptoms: -headache -dizziness or vertigo -lack of awareness of surroundings -nausea and vomitting Late: -persistent low grade headaches -light headed -poor attention and concentration -memory dysfunction -fatigue -irritable -intolerance to bright lights and loud noises -anxiety/depression -sleep disturbance |
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Concussion pathogenesis
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Pathogenesis unknown
-Depolarization due to excitatory-amino- acid-mediated ionic fluxes across cell membranes -Depletion of mitochondrial ATP -Alterations in vascular permeability |
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Brain swelling in trauma
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Poorly understood
May be due to edema, increased blood volume, or both, presumed to be secondary to impaired autoregulation or vasomotor control Does not necessarily correlate with severity of injury Especially common in children May be diffuse or focal adjacent to hemorrhage |
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Mortality from head injury
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Inversely related to GCS
-GCS = 15 <1%, GCS = 4-5 <50%, GCS = 3 80% Inversely related to age, if comatose Intracranial pressure, if comatose -< 20 mmHg = 15% -> 20 mmHg, reducible = 45% -> 20 mmHg, not reducible = 90% Diffuse swelling and shift of midline on imaging associated with worse prognosis Type of injury: EDH (5-15%), GSW (55%), Acute SDH (simple 20-25%, complicated 40-75%, bilateral 75-100%) |
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Head injury acute complications
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Persistent CSF leak infection risk
Pneumocephalus: usually asymptomatic Carotid-cavernous fistula -Laceration of internal carotid artery in the cavernous sinus -Pulsating exophthalmos, ocular chemosis, orbital bruit +/- CN palsies (III,IV,V1,VI) Vascular injury dissection thrombosis thromboembolic stroke Dural sinus thrombosis Infarcts related to herniation: -ACA: compressed with subfalcine herniation -PCA: compressed with transtentorial herniation Cranial nerve injury: -Seen most often with basilar skull fracture -Facial nerve most common (0.3 – 5% of injuries) Infections |
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Head injury long term complications
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Persistent neurological deficits related to brain injury
Post-concussive syndrome (see earlier slide) Post-traumatic epilepsy Prognosis in prolonged coma due to trauma -50% of adults and 60% of children who are comatose for 30 days will recover consciousness within one year (meaning, able to follow commands consistently) -Only 15% of comatose patients will recover consciousness in coma from non-traumatic causes (e.g., post-cardiac arrest) |
