Neurosensory System: Vasculature of the CNS PDF

Neurosensory HARC Lecture 1 -- Vasculature of the CNS Describe and differentiate between the cerebral, cerebellar and brainstem arterial supply and trace their origin and anastomosis There are 3 arteries that supply the neck and head, which originate from 2 different sources. **Common Carotid** (...

Neurosensory HARC Lecture 1 -- Vasculature of the CNS Describe and differentiate between the cerebral, cerebellar and brainstem arterial supply and trace their origin and anastomosis There are 3 arteries that supply the neck and head, which originate from 2 different sources. **Common Carotid** (Bifurcation at C4) - Internal Carotids - External Carotids -- predominantly extracranial structures (face and scalp), with the exception of the middle meningeal artery (intracranial) **Subclavian Artery** - Vertebral Arteries  **[The Arterial Supply to the Cerebrum, Cerebellum and Brainstem]** There is an **anterior (Carotid) system**, and a **posterior (Vertebrobasilar) system** -- they are connected by the Cerebral Arterial Circle (Circle of Willis). This connection is called a **natural circulatory arterial anastomosis**. The Carotid System is formed by the right and left ICA. - The ICA enters cranium via the carotid canal -- it passes over the **foramen lacerum** (indicated by the red circle). The foramen lacerum is covered by a membrane -- this gives the ICA room to dilate, instead of pressing up against bone - It then undergoes two characteristic 90^o^ bends called the carotid siphon The Vertebrobasilar System is formed by the vertebral arteries joining to form the Basilar artery - The vertebral arteries are branches of the subclavian arteries, and run through the transverse foramina of the vertebrae before entering the skull via the **foramen magnum** - They join to form the basilar artery which runs along the anterior surface of the brainstem, and lies on top of the **clivus** of the cranial base (it is the basilar part of the occipital bone) **[The Circle of Willis]** Note that the **communicating** arteries are *not* for passage of blood from one side of the brain to the other. This is logical, because in theory, blood comes up via both vertebral arteries and both internal carotid arteries *under the same pressure* -- this equalises the pressure on both sides. Therefore, if you were to inject a contrast agent in e.g. the right common carotid, it is unlikely that it would travel via *anterior communicating artery* to show on the left side of the brain. Similarly, it is unlikely that it would travel via the *posterior communicating artery* and use the basilar artery to show the posterior aspect of the brain. This means that the *communicating arteries* are anastomoses which are used under *occlusion only.* **[The Anterior Cerebral Artery (ACA)]** - It passes underneath the corpus callosum and progresses by doubling back on itself superiorly and posteriorly along the superior surface of the corpus callosum. - Supplies: - Frontal lobe - Medial aspect of the parietal lobes - Motor-cortex (for lower limb only) - Parts of the basal ganglia (e.g. parts of the putamen and caudate nucleus) and part of the anterior limb of the internal capsule **[The Middle Cerebral Artery (MCA)]** - Passes laterally towards the temporal lobe onto the lateral aspects of the cerebrum - It is the terminal branch of the ICA - Supplies: - Temporal lobe - Parietal lobe - Broca's and Wernicke's Speech areas - Parts of the basal ganglia and part of the internal capsule **[The Posterior Cerebral Artery (PCA)]** - Terminal branch of the basilar artery - Passes posteriorly to the parietal lobe - Supplies: - Occipital lobe (visual cortex) **[Important Branches of the Cerebral Arteries ]** There are branches of the large cerebral arteries which supply deep brain structures, such as the basal ganglia. The most important are the lateral striate arteries from the MCA and the medial striate arteries from the ACA.  **Lateral Striate Arteries -- from MCA** - Also called the Lenticulostriate arteries -- these arteries are seen as 'arteries of stroke' - Arise from the first part of the MCA (M1 segment) - Supplies parts of the anterior thalamus, basal ganglia (putamen, pallidus, caudate nucleus) and superior half of the internal capsule - Small vessel disease (e.g. atherosclerosis) will cause spontaneous intracerebral haemorrhage and lacunar infarctions -- classical motor and sensory presentations **Medial Striate Artery -- from ACA** - Also called the recurrent artery of Heubner - Supplies the antero-inferior aspect of the internal capsule **Choroidal Arteries (supply the choroid plexuses)** - Anterior (MCA) -- first branch; supplies the postero-inferior aspect of the internal capsule - Posterior (PCA) -- multiple branches **[The Cerebellar Arteries]** SCA -- passes back over the midbrain AICA -- passes back over the pons PICA -- passes back over the medulla oblongata As they pass over, they supply them with blood -- therefore, occlusions affect not only the cerebellum but the brain stem. The flocculonodular lobe is primarily supplied by the AICA (gold) and the anterior and posterior lobes have a divide between them which is supplied by the SCA and PICA. **[The Meningeal Arteries]** The main meningeal artery is the **middle meningeal artery** which passes through the foramen spinosum. It originates as the external carotid artery, which branches into the maxillary artery. The maxillary artery then gives rise to the **middle meningeal artery**. The pterion is the link between 4 bones of the skull. The meningeal artery lies inside of it. As a result, the pterion is prone to fracture and the meningeal artery is prone to damage -- it is a common cause of traumatic epidural haemorrhage. Describe cerebrospinal fluid (CSF) circulation and abnormities that may interrupt the flow of CSF Embryologically the ventricles are derived from different ventricles: - Telencephalon -- lateral ventricles - Diencephalon -- 3^rd^ ventricle - Metencephalon -- upper 4^th^ ventricle - Myelencephalon -- lower 4^th^ ventricle Note that the ventricles are not true structures -- they are actually just the negative spaces in between brain tissue structures and are filled with CSF. The CSF is produced by the choroid plexuses of each ventricle -- a choroid plexus is a group of vascularised pia mater. The lateral ventricles are connected to the 3^rd^ by the intraventricular foramina (Foramen of Monro). The 3^rd^ ventricle is connected to the 4^th^ by the cerebral aqueduct of the midbrain (Foramen of Sylvius). The 4^th^ ventricle has lateral apertures (Foramen of Luschka) and a median aperture (Foramen of Magendie) which leak the CSF out into the subarachnoid space -- it sits between the brain stem and the cerebellum. **[Functions of CSF]** Buoyancy 🡪 The brain has a true mass of 1.4kg, but when floating in CSF, its net weight is 25g. This allows the brain to maintain its density without crushing its own blood vessels and neurons under its own weight **Chemical Stability** 🡪 CSF rinses metabolic waste from the CNS through the BBB; important for controlling pH **Prevents Brain Ischaemia** 🡪 Achieved by reducing the volume of CSF inside the box of the skull; decreases total ICP and facilitates CBF **[Subarachnoid Cisterns]** These are dilations of the subarachnoid space (particularly in the lumbar area, near the cauda equina). CSF fills this space and supports the spinal cord. The **cisterna magna** is the largest cistern (where CSF moves into when it comes out of the 4^th^ ventricle), but there is also the pontine cistern, the cerebellopontine cistern and the interpeduncular cistern (around the pituitary). After having circulated in the subarachnoid space, CSF drains into the dural venous sinuses via **arachnoid granulations**. It can also be absorbed by tissue or drain through cranial fossa. The majority of CSF problems are due to prevention of reabsorption of CSF which results in high intracranial pressure. Define and describe the dural venous sinuses and their venous flow pattern  The end destination for all of this blood is the internal jugular vein -- this descends in the neck inside the carotid sheath, alongside the carotid artery and CN X. **[Dural Venous Sinuses]** The dural venous sinuses are the spaces between the two layers of the dura mater -- venous blood collects in these spaces and drains away. The two layers of the dura mater are: - The periosteal layer -- fixed to the internal side of the skull, and fix down the meningeal arteries which are deep to it - The meningeal layer which has reflections through the brain i.e. falx cerebri, falx cerebelli, tentorium cerebelli. The two layers are fixed together except at the point of these reflections -- blood collects and is drained away. The meningeal layer of the dura mater blends in with the adventitia (tunica externa) of these veins, therefore, these veins could also be seen as negative space created by the two layers of dura mater. The confluence of sinuses is the point where the majority of them join near the occipital bone. The blue circle indicates the point where the IJV is formed. It leaves via the jugular foramen (CN IX, X and XI also leave via here). **[The Cavernous Sinus]** Describe how a haemorrhage or blockage could disrupt the flow of arterial, venous or CSF flow and the resulting implications +-----------------+-----------------+-----------------+-----------------+ | | **Epidural | **Subdural | **Subarachnoid | | | Haemorrhage** | Haematoma** | Haemorrhage** | +-----------------+-----------------+-----------------+-----------------+ | Location | Bleeding | Venous blood | Bleeding | | | *quickly* | *slowly* builds | between the | | | between the | in the space | arachnoid mater | | | calvarium and | between the | and the pia | | | the | *meningeal* | mater -- the | | | *periosteal* | *dura* and the | **subarachnoid* | | | dura mater -- | *arachnoid* | * | | | the **epidural | mater -- the | space | | | space.** | **subdural | | | | | space.** | | | | Most commonly a | | | | | skull fracture | | | | | at the pterion | | | | | which ruptures | | | | | the MCA | | | +-----------------+-----------------+-----------------+-----------------+ | Mechanism | Laceration to a | Traumatic *or* | Usually caused | | | meningeal | non-traumatic | by the rupture | | | artery -- most | rupture of a | of a **(Berry) | | | commonly the | **bridging | aneurysm** -- | | | **middle | vein** -- a | the most | | | meningeal | vein that | commonly | | | artery,** if it | drains cerebral | affected vessel | | | is a fracture | veins into the | is the **middle | | | at the pterion. | dural venous | cerebral | | | | sinuses. A | artery.** | | | | common example | | | | | are the veins | | | | | draining into | | | | | the **superior | | | | | sagittal | | | | | sinus.** | | +-----------------+-----------------+-----------------+-----------------+ | **CT Findings** | Well-defined, | A | A | | | **biconvex** | banana/**cresce | characteristic | | | (crescent-shape | nt-shaped | **star-shape**, | | | d) | hyper-density** | as blood fills | | | **hyperdense** | between the | the | | | area between | brain and | **subarachnoid | | | the calvarium | calvarium that | cisterns**, | | | and brain. Most | is **not | where only CSF | | | likely located | limited by | should be. | | | around the | suture lines,** | | | | pterion and is | and so may | | | | **sharply | **shift the | | | | demarcated**. | ventricles** -- | | | | | this appears | | | | May also see a | with a crescent | | | | skull fracture. | shape. | | | | It is **limited | | | | | by suture | | | | | lines**. | | | +-----------------+-----------------+-----------------+-----------------+ | **CT** |  | 18.png) | | +-----------------+-----------------+-----------------+-----------------+ | **Clinical | An initial | Takes weeks to | Will likely end | | Features / | **lucid | develop, as the | in a stroke, | | Symptoms** | interval** | vein is under | but you know if | | | followed by | low pressure. A | the stroke has | | | **sudden acute | clot is likely | been caused by | | | onset.** | to build, | a subarachnoid | | | | rather than an | haemorrhage | | | Begins to press | active bleed. | because they | | | on the temporal | There is an | will first have | | | lobe (e.g. | **increasing | a **thunderclap | | | Broca's Area) | headache,** and | headache and** | | | and so will | **changes in | will **vomit** | | | have difficulty | mood.** High BP | and then | | | with speech, | and low pulse. | **faint** due | | | breathing and | | to the high | | | erratic mood | Focal deficits, | pressure in the | | | swings -- | e.g. | brain, before | | | mistaken for | contralateral | having a | | | being drunk. | hemiparesis, | **stroke**. | | | | sensory loss | | | | Focal deficits | | | | | e.g. | | | | | contralateral | | | | | hemiparesis, | | | | | sensory loss. | | | | | | | | | | If the temporal | | | | | lobe herniates | | | | | through the | | | | | tentorial notch | | | | | -- presses on | | | | | CN III 🡪 CN III | | | | | palsy | | | +-----------------+-----------------+-----------------+-----------------+ | **Management** | Burr hole can | Burr hole can | Clipping of the | | | be used to | be used to | aneurysm | | | drain it but | drain it but | | | | may require a | may require a | | | | craniotomy if | craniotomy if | | | | the blood has | the blood has | | | | coagulated | coagulated | | +-----------------+-----------------+-----------------+-----------------+ **[Strokes]** Any sort of cerebrovascular accident -- there are 2 main types; ischaemic and haemorrhagic. There has to be a deprivation of blood supply to brain tissue to be classed as a stroke. +-----------------------------------+-----------------------------------+ | **Ischaemic Stroke** | **Haemorrhagic** | +-----------------------------------+-----------------------------------+ | A blockage prevents blood supply | Bleeding in or around the brain | | to brain tissue, resulting in | tissue | | ischaemia and potentially | | | infarction. | | +-----------------------------------+-----------------------------------+ | Types include: | Types include: | | | | | - Embolism -- an embolus | - Intraventricular haemorrhage | | travels from somewhere else | | | in the body and occludes a | - Intraparenchymal haemorrhage | | cerebral blood vessel | | | | - Subarachnoid haemorrhage | | - Thrombosis -- the clot forms | | | in the cerebral vessel | | | itself, typically due to the | | | rupture of an atherosclerotic | | | plaque | | | | | | - Cerebral Venous Sinus | | | Thrombosis (CVST) -- a clot | | | in the dural venous sinuses, | | | which results in venous | | | congestion | | | | | | - Systemic Hypoperfusion | | +-----------------------------------+-----------------------------------+ **[Transient Ischaemic Attacks (TIAs)]** This is a *transient* focal neurological deficit that is caused by **ischaemia, not infarction**. This means that a TIA is completely reversable, whereas a stroke *is not.* It typically resolves in less than 24 hours, but TIAs are risk factors for strokes later in life. The symptoms are highly dependent on what vessel is affected, but the following are common: - Amaurosis fugax 🡪 temporary loss of vision in one or both eyes due to lack of blood supply - Contralateral hemiparesis - Aphasia, dysarthria, confusion **[Cavernous Sinus Syndrome or Thrombosis]** Infection to the superficial veins of the face could pass back to the structures of the cavernous sinus and cause a lot of swelling.   **[Hydrocephalus]** Too much CSF -- often caused by an inability to drain rather than overproduction. Presents firstly with large headaches as the ventricles swell and push on the structures surrounding them. If you cannot find a cause (idiopathic hydrocephalus) or cannot remove the obstruction, then a shunt is put in place where the CSF drains into the abdomen. Neurosensory HARC Lecture 2 -- The Motor System -- Clinico-Anatomical Correlations Define the components of the basal ganglia -- the nuclei and pathways The basal nuclei *receive* *input* from the cerebral cortex and *provide* *output* to the motor parts of the cortex via the medial and ventral group of nuclei of the thalamus. A major function of the nuclei is to **adjust amplification of movement.** **The basal ganglia can be described in different ways: anatomically, or into 4 loops of common functions, or into pathway involvement.**  **[Discussing the Basal Ganglia by Anatomy]** **Components of the Basal Nuclei System** **Striatum** = Caudate Nucleus + Putamen **Pallidum** = GPi + GPe **Subthalamic Nuclei** **Substantia Nigra** - Reticular region - Compact region **The Internal Capsule** The internal capsule runs between the thalamus and the basal nuclei. It is a white matter tract pathway that is boomerang shaped in a transverse section. - The structures that are lateral to it are the Pallidum and Putamen (P) - The structures that are medial to it are the Caudate Nucleus (CN) and the Thalamus (T)  In a transverse view, it has an anterior limb and a posterior limb, connected by the genu (a bend) - Anterior limb - Frontopontine and Thalamocortical fibres - Genu - Corticobulbar / Corticonuclear tract (motor signals for cranial nerves) - Posterior limb - Corticospinal tract (motor signals) - Arms, Trunk, Lower Limb (ATL) The routes of the right and left corticospinal tracts through the internal capsule. They decussate inside the medulla oblongata, providing contralateral innervation. **Vasculature of the Internal Capsule** In a lateral view, the internal capsule will appear as a rectangle. Superior Half 🡪 Lateral striate branches from MCA Inferior Half Anterior Limb 🡪 Medial striate branch from ACA Inferior Half Genu 🡪 ICA branches Inferior Half Posterior Limb 🡪 Anterior choroidal from MCA - However, there is a lot of overlap. **[Discussing the Basal Ganglia by Pathway Involvement ]** Basal ganglia are responsible for modulating the influence of thalamic activity on the motor cortex. The basal ganglia can be categorised according to where they are involved in the direct and indirect pathways. **Striatum** = Input **Nigrostriatal** = Modulation **Pallidus** = Output **Direct Pathway of the Basal Nuclei** 🡪 Allows wanted movement *N.B. All excitatory signals are sent via the neurotransmitter [glutamate]. All inhibitory signals are sent via [GABA].* 1. At, rest, **the GPi inhibits the thalamus**. Since the thalamus excites the motor cortex, inhibiting it at rest will prevent unwanted movement. 2. The motor cortex then desires movement 🡪 an impulse is sent down an **excitatory axon** to the **striatum**. Inside the striatum, it synapses with an **inhibitory neuron** that will travel to the GPi. 3. Excitation of the striatum = **inhibition of GPi** 4. Now that the GPi is inhibited, the thalamus is free to send **excitatory signals** to the motor cortex 5. **Muscles move** as instructed by the motor cortex, via motor pathways 6. At the same time, the **subthalamic nucleus** **excites** the **substantia nigra** 7. The substantia nigra released **[dopamine]** onto **[DA 1 receptors]** **on the inhibitory neurons** inside the striatum. This excites the inhibitory striatum neurons, thereby *further inhibiting the GPi*. **Indirect Pathway of the Basal Nuclei** 🡪 Prevents unwanted movement *N.B. Similar to the* Direct Pathway, *excitatory signals are sent using the neurotransmitter glutamate. Inhibitory, GABA.* 1. At rest, the GPi inhibits the thalamus. This prevents unwanted movement. 2. When the motor cortex wants to inhibit a specific movement, is sends signals via an excitatory axon to the **striatum**, where it synapses with an inhibitory neuron which will go to the GPe 3. Excitation of the striatum = inhibition of the GPe 4. At rest, the GPe is usually inhibiting the subthalamic nucleus. However, now that the GPe itself is inhibited; it can no longer inhibit the subthalamic nucleus. The subthalamic nucleus is now free to send impulses 5. The subthalamic nucleus excites the GPi 🡪 this further inhibits the thalamus, further preventing movement 6. When movement *is* desired, the subthalamic nucleus can also stimulate the substantia nigra 7. The substantia nigra uses **[dopamine]** on **[DA 2 receptors]** on the inhibitory axons coming out of the striatum. This means that **step 3 is inhibited** 🡪 the GPe is no longer inhibited 8. GPe no longer inhibited 🡪 subthalamic nucleus is inhibited by the GPe 🡪 the GPi is not excited by the subthalamic nucleus 🡪 the thalamus is not inhibited by the GPi = the thalamus is free to send excitatory signals to the motor cortex 9. The motor cortex innervates muscles via motor pathways 10. Note that the subthalamic nucleus can also work backwards to inhibit the subthalamic nucleus, thereby preventing steps 7, 8 and 9 **Summary of the Pathways of the Basal Nuclei** The basal nuclei can interact with the motor cortex via 2 pathways; **direct** or **indirect.** **Direct Pathway** - - **Indirect Pathway** - - **[Discussing the Basal Ganglia by Loops]** **[Basal Ganglia Disorders]** These are primarily caused by an imbalance between the two output systems -- the direct and indirect pathways. **Hypokinetic** -- Parkinson's - **Excess indirect output,** limited direct output - Movement is being depressed too much - Typically, idiopathic/sporadic - Pars compacta of the substantia nigra is lost 🡪 lowers dopamine in the striatum **Hyperkinetic** -- Huntington's - **Excess direct output,** limited indirect output - Movement is being stimulated too much - Autosomal dominant -- mutation of the Huntingtin protein - Neurodegenerative (progressive) - It is a result of the caudate nucleus degenerating (resulting in large lateral ventricles), which means a loss of input and also D2 receptors 🡪 there is not enough indirect pathway stimulation Define and describe the difference between an upper motor neuron and a lower motor neuron ---------------------------------------------------------- -------------------------------------------------------------------------------------------------------------------------------------- **Upper Motor Neuron** **Lower Motor Neuron** The entire cell (soma and axon) is inside the CNS The soma is located in the spinal cord's grey matter or within cranial nuclei (inside the CNS). The axon extends outside of the CNS. Transmits motor impulses from the cerebral cortex to LMN Transmits impulses from UMN to the skeletal muscle Soma is relatively larger Soma is relatively smaller Classified based on the pathway they travel in Classified by the type of muscle fibre they innervate Synapse onto LMN Synapse on to target muscles ---------------------------------------------------------- -------------------------------------------------------------------------------------------------------------------------------------- **Types of Motor Tracts** Pyramidal Tracts 🡪 these are for the generation of voluntary movement Extrapyramidal Tracts 🡪 these are for the coordination of voluntary movement **Pyramidal Tracts** 🡪 - Corticobulbar 🡪 head and neck - UMNs synapse in the brainstem in the nuclei of CNs - The LMN is carried in the cranial nerves - Corticospinal 🡪 trunk and limbs - Decussate in the pyramids in the medulla - Synapse with an LMN at the required vertebral level in the anterior horn - The LMN is carried in spinal nerves  **Extrapyramidal Tracts** 🡪 These are other tracts which can influence or coordinate movement e.g. reticulospinal tract but cannot directly initiate movement. The extrapyramidal system also includes structures such as: - Cerebellum, for balance and posture - Basal ganglia, for selection of movement - Nigrostriatal pathway, for movement production **A Summary of Pyramidal and Extrapyramidal Tracts** Define and describe the difference between an upper motor lesion and a lower motor lesion and their implications ------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------ ---------------------------------------------------------------------------------------------------------- **Lesions of UMNs** **Lesions of LMNs** **Spasticity** (*velocity-dependent* and *clasp-knife reflex*) Hypotonia Hyperreflexia (refers to monosynaptic tendon reflexes. Hyperreflexia occurs because of the loss of the descending pathways which modulate/inhibit excess these reflexes) Hyporeflexia Only affect pyramidal tracts 🡪 Loss of voluntary movement, but tone, coordination and posture are maintained Affect pyramidal and extra-pyramidal tracts 🡪 Loss of voluntary movement, tone, coordination and posture No muscle wasting **Muscle wasting** may be present No fasciculations **Fasciculations** may be present Loss of superficial reflex (reflexes against scraping of the skin) (e.g. abdominal, cremasteric) (*not* mono-synaptic, involve the brain) Superficial reflexes are preserved Positive Babinski sign 🡪 scrape an object along the lateral aspect of the sole of the foot. Normally, the toes should curl downwards to the floor (flexion). A positive Babinski's sign would be the toes flexing backwards/fanning out. ------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------ ---------------------------------------------------------------------------------------------------------- Describe how cranial nerve abnormalities can manifest -- trigeminal neuralgia, facial palsy and disorders of the eye  **[Disorders of the Eye (CN III, IV and VI)]** +-----------------+-----------------+-----------------+-----------------+ | | **CN III | **CN IV Palsy** | **CN VI Palsy** | | | Palsy** | | | +-----------------+-----------------+-----------------+-----------------+ | **Muscles | Superior | Superior | Lateral rectus | | Affected** | rectus, | oblique | | | | Inferior | | | | | rectus, Medial | | | | | rectus, | | | | | Inferior | | | | | oblique, | | | | | sphincter | | | | | pupillae, | | | | | levator | | | | | palpebrae | | | | | superioris | | | +-----------------+-----------------+-----------------+-----------------+ | **Causes** | Ischaemia | Diabetes | Diabetes | | | | Mellitus, | Mellitus | | | - Would spare | | | | | the pupil | Hypertension | Hypertension | | | as the | | | | | motor | Trauma | Raised ICP | | | fibres | | | | | would be | Tumour | | | | more | | | | | affected | | | | | than the | | | | | parasympath | | | | | etic | | | | | fibres | | | | | | | | | | Uncal | | | | | Herniation | | | | | | | | | | Aneurysm of | | | | | Posterior Comm. | | | | | Artery | | | | | | | | | | Cavernous Sinus | | | | | Thrombosis | | | | | | | | | | Midbrain stroke | | | +-----------------+-----------------+-----------------+-----------------+ | **Effect** | **Motor | **Vertical | **Horizontal | | | Dysfunction** | Diplopia** | Diplopia** | | | | | | | | - "Down and | **The** pupil | The affected | | | Out" turn | of the affected | eye is unable | | | of eyes | eye is higher 🡪 | to abduct and | | | | the head tends | is displaced | | | - Ptosis | to tilt to the | medially in | | | | unaffected side | primary | | | **PNS | to compensate | position of | | | Dysfunction** | for the lack of | gaze | | | | intorsion | | | | - Pupil does | | | | | not | - Difficulty | | | | constrict | going down | | | | to light 🡪 | the stairs; | | | | blown out | reading | | +-----------------+-----------------+-----------------+-----------------+ | **Examples** | |  | | +-----------------+-----------------+-----------------+-----------------+ **[Disorders of CN V]** +-----------------------------------+-----------------------------------+ | **Supranuclear (UMN) or Nuclear | **Lesion of CN V Peripheral | | Lesions of CN V** | Nerves** | +-----------------------------------+-----------------------------------+ | Lesion of the Sensory Nuclei 🡪 | **Ophthalmic Nerve (CN V~1~)** | | Ipsilateral loss of sensation to | affected; | | that half of the face | | | | - Absent corneal reflex | | | | | | Anaesthesia of the forehead | +-----------------------------------+-----------------------------------+ | Lesion of the Motor Nuclei 🡪 | **Maxillary Nerve (CN V~2~)** | | Ipsilateral weakness of the | affected; | | muscles of mastication and | | | anterior 2/3 of tongue | Anaesthesia of the mid-face | +-----------------------------------+-----------------------------------+ | | **Mandibular Nerve** **(CN | | | V~3~)** affected; | | | | | | - Sensory 🡪 anaesthesia of the | | | lower face | | | | | | - Motor (LMN) 🡪 anterior 2/3 | | | paralysed, and the muscles of | | | mastication are flaccid). The | | | jaw tends to deviate to the | | | *side of the lesion*, because | | | of unopposed action from the | | | opposite pterygoid muscle | +-----------------------------------+-----------------------------------+ +-----------------------+-----------------------+-----------------------+ | | **Supranuclear (UMN) | **Peripheral (LMN) | | | Lesions of CN VII** | Lesions of CN VII** | | | | | | | **(Central)** | **(Peripheral)** | +-----------------------+-----------------------+-----------------------+ | Area Affected | A unilateral UMN | Ipsilateral weakness | | | lesion which causes | of the *forehead* | | | contralateral | (incl. eyelids), | | | weakness of the | mid-face and lower | | | mid-face and lower | face | | | face | | | | | - Note that | | | - Forehead sparing | forehead sparing | | | 🡪 the phenomenon | is *not present* | | | by which the | | | | forehead is | Can present with | | | spared because it | sensory or autonomic | | | is inn ervated | symptoms too: | | | ipsilaterally | | | | | - Pain | | | | | | | | - Inability to | | | | taste using | | | | anterior tongue | +-----------------------+-----------------------+-----------------------+ | Presentation | Present | Present *Ipsilateral* | | | *Contralateral* to | to the Lesion | | | Lesion | | | | | - Inability to | | | - Mouth drooping | frown | | | | | | | | - Inability to | | | | blink | | | | | | | | - Mouth drooping | +-----------------------+-----------------------+-----------------------+ | Causes | - **Infection** 🡪 | - **Acute | | | Herpes Zoster | Idiopathic** 🡪 | | | (Ramsey Hunt | peripheral nerve | | | Syndrome) | palsy is termed | | | | **Bell's Palsy** | | | - **Tumours** | and is the | | | | primary cause of | | | - 'Any' brain | peripheral CN VII | | | lesion which | nerve palsy | | | affects the | | | | supranuclear | - **Trauma** 🡪 | | | tract or it's | Temporal Bone | | | nuclei in the | fracture | | | pons | | | | | - **Tumours** 🡪 | | | | Particularly the | | | | parotid gland | +-----------------------+-----------------------+-----------------------+ **[Disorders of CN VII]** **[Disorders of CN IX, X, XI, XII (Bulbar Palsies)]** +-------------+-------------+-------------+-------------+-------------+ | | **CN IX | **CN X | **CN XI | **CN XII | | | (LMNs)** | (LMNs)** | (LMNs)** | (LMNs)** | +-------------+-------------+-------------+-------------+-------------+ | **Cause** | Often | Trauma | Surgery of | Tumours | | | unknown, | | the | | | | may be a | Diabetes | cervical | Trauma | | | compression | | region | | | | of a blood | Tumours | (travels | | | | vessel | | primarily | | | | | | through the | | | | | | spine, so | | | | | | is less | | | | | | vulnerable) | | +-------------+-------------+-------------+-------------+-------------+ | **Presentat | - Gag | - Gag | - Paresis | - Atrophy | | ion** | reflex | reflex | of | and | | | absent | absent | sternoc | fascicu | | | | | leidomastoi | lation | | | - Soft | - Soft | d | of the | | | palate | palate | muscle | tongue | | | weaknes | weaknes | -- in | | | | s | s | health, | - The | | | 🡪 | 🡪 | the SCM | tongue | | | deviati | deviati | turns | deviate | | | on | on | the | s | | | of the | of the | head | to the | | | uvula | uvula | the | side of | | | towards | towards | opposit | the | | | the | the | e | lesion | | | opposit | opposit | way. | when | | | e | e | Therefo | protrud | | | side | side | re, | ed | | | | | in | | | | - Loss of | - Nasal | paresis | | | | taste | speech | , | | | | on | | there | | | | posteri | - Vocal | is | | | | or | cords 🡪 | weaknes | | | | 1/3 of | dysarth | s | | | | tongue | ria | turning | | | | | | the | | | | | - Epiglot | head | | | | | tis | the | | | | | paralys | contral | | | | | is | ateral | | | | | 🡪 | way too | | | | | aspirat | | | | | | ion | - Paresis | | | | | | of | | | | | | trapezi | | | | | | us | | | | | | -- | | | | | | shoulde | | | | | | r | | | | | | droopin | | | | | | g | | | | | | and | | | | | | winging | | | | | | of the | | | | | | scapula | | | | | | on the | | | | | | ipsilat | | | | | | eral | | | | | | side | | +-------------+-------------+-------------+-------------+-------------+ Note that the above table summarises **Bulbar Palsies** 🡪 lesions which affect the LMNs of medullary CNs. If the lesions were supranuclear, then these would be termed **pseudo-bulbar palsies** and whilst the same regions would be affected, the motor symptoms would be UMN symptoms, rather than LMN symptoms. Note that CN IX, X and XII are all implicated in **Jugular Foramen Syndrome** and their LMN features would present together. Be able to trace the pathways of the major sensory and motor pathways through the spinal cord, brainstem, cerebellum and cerebrum **2 Motor (Descending) (Pyramidal Only)** - - - - - - Voluntary movement for head and neck - Runs through genu of the internal capsule - Decussation Points - Midbrain -- CN III, CN IV - Pons -- V, VI, VII - Medulla -- IX, X, XI, XII **3 Sensory (Ascending)** - - Pain, temperature, touch, pressure - Anterior tract 🡪 crude touch, pressure - Lateral tract 🡪 pain, temperature, crude touch - Decussate as they enter the spinal cord at their vertebral level - - Conscious proprioception, touch, vibration - Cuneate Fasciculus -- upper limb afferents - Gracile Fasciculus -- lower limb afferents - Note that the tract is referred to as 'dorsal columns' (fasciculi) when in the spinal cord and is referred to as 'medial lemnisci' when it's in the brain stem. They are the same structure, just referred to as different things when in different locations. - - Non-conscious proprioception - Ventral tract 🡪 enters via superior cerebellar peduncle - Dorsal tracts 🡪 enters via the inferior cerebellar peduncle