Brainstem Motor 3 Lecture Notes (DO-SYS-725)

Brainstem Motor 3 Common syndromes and some sensory nuclei DO-SYS-725 Med Neuro II Lecture 8 - Tony Harper, Ph.D Thursday Jan 23 @11am 1 Learning Objectives I can explain the functions of the sensory nuclei of the trigemin...

Brainstem Motor 3 Common syndromes and some sensory nuclei DO-SYS-725 Med Neuro II Lecture 8 - Tony Harper, Ph.D Thursday Jan 23 @11am 1 Learning Objectives I can explain the functions of the sensory nuclei of the trigeminal nerve, and Identify the location of neuron cell bodies for the sensory fiber tracts within the brainstem I can recognize and describe the distribution of vertebrobasilar arterial branches to the different regions of the brainstem I can diagnose common syndromes involving the pons and medulla given a patient history and list of symptoms I can predict the level of a lesion producing gaze/cranial nerve disorders with associated with alternating hemiplegia I can diagnose the level of a brainstem lesion in a comatose patient based on body posturing and breathing pattern 2  Trigeminal Mesencephalic trigeminal nucleus sensory Involved in proprioception related to muscles nuclei of mastication. Primary (1°) afferent cell bodies of pseudounipolar neurons are located within the nucleus (not the trigeminal ganglion). Sends fibers to cerebellum through superior cerebellar peduncle. Chief/Primary trigeminal sensory nucleus Relays fine touch/discriminative sensation and pressure. Contains 2° afferent cell bodies. Spinal trigeminal nucleus Conveys crude touch, pain, and temperature. Contains 2° afferent cell bodies. Contiguous with substantia gelatinosa in spinal cord Neuroanatomy in Clinical Context (9 th ed.), Haines., 6-2 3  Trigeminal 1st Order Sensory Neurons Trigeminal/Gasserian Ganglion (not Gassler-ian) Proprioception reflexes Trigeminal Nerve Rootlet Trigeminal Nerve Fine-Touch 1 st Order Neurons make Spinal Pain/Temperature Trigeminal Tract before synapsing Lesion Mesencephalic Nucleus: Lose jaw muscle proprioception It is continuous with Lissauer’s (e.g. may crack teeth while chewing), and will not have “Jaw Jerk Tract in spinal cord Reflex” (may not have anyway though) Includes sensory fibers from Lesion Chief Trigeminal Nucleus: Ipsilateral loss of fine touch cranial nerves 7, 9 and 10 also Lesion Spinal Trigeminal Nucleus: ipsilateral loss of pain and temperature. Lose Direct and Consensual Corneal and Lachrymal reflexes Lesion in area around trigeminal ganglion: Paratrigeminal (Raeder) Syndrome – miosis, ptosis, facial pain, jaw weakness. Usually CNs 3,4,6 and postganglionic sympathetics are affected 4  Trigeminal 2nd Order Sensory Neurons VPM 2nd Order Fine Touch Trigeminal ascends ipsilateral in lemniscus Dorsal Trigeminal Tract Fine-Touch Pain/Temperature Lesion Spinal Trigeminal Tract: ipsilateral loss of pain/temp in face Lesion trigeminal lemniscus: Bilateral, 2nd Order Pain and asymmetrical sensory disassociation Temperature ascends Lesion VPM: Similar to trigeminal contralateral in lemniscus plus hypogeusia( loss of Ventral Trigeminal taste, mostly contralateral), and Tract possible “thalamic pain syndrome” 5 Spinal Trigeminal Tract Trigeminal Neuralgia (Tic Douloureux) involves (usually unilateral) spontaneous pain over the trigeminal sensory area. Caused by irritation of CNV, by compression by blood vessels (e.g. superior cerebellar a.), tumors, bruxism, etc. One treatment option is to sever the ipsilateral spinal trigeminal tract. Lesion of spinal trigeminal tract – has “dermatomes” that spread out from mouth in “onion skin” pattern. Mouth fibers terminate closer to obex, back of headfibers near cervical cord Neuroanatomy through Clinical Cases (2 ed ed), Blumenfeld, Fig 12.9 6 Trigeminal Reflexes Bisynaptic reflex, Should result in fast bilateral blinking (direct Jaw Jerk Reflex: Corneal (Blink) Reflex: and consensual) Afferent Limb: V1 Opthalmic N. (Nasociliary Br) Efferent Limb: Facial Motor Nucleus to Facial N. (to orbicularis occuli) Monosynaptic myotactic stretch reflex, will cause a quick contraction of masseters. Afferent and Efferent Limbs: V3 mandibular N. Tests integrity of Trigeminal Motor Nucleus and Trigeminal Mesencephalic Nucleus Normally reduced or absent in healthy patients. Becomes hyper-reflexive with UMN damage to corticobulbar tract. Is example of a pathological reflex Helps to distinguish trigeminal motor nucleus lesions from corticobulbar brain lesions 7 Alternating hemiplegia Note: this lesion does not reach PPRF, and so only has Basic Clinical Neuroscience (3rd ed.) Fig. 27-5 a unilateral effect 8  R L FEF Right cortex Eyes deviate: Right Eyes deviate: Right UMN signs: Left UMN signs: Right 9  Left Frontal Left Abducens Eye Field and Nucleus and Left Left Primary Corticospinal Motor Cortex Tract Neuroanatomy through Clinical Cases (2 ed ed), Blumenfeld, Fig 13-15 10 Brainstem Vascular Supply Blood supply to the brain can be divided into two categories: Ø Anterior circulation – supplied by the internal carotid arteries. Ø Posterior circulation – supplied by the Internal vertebral arteries. carotid a. Posterior circulation (AKA “vertebrobasilar system”) is the primary supply of the brainstem. Vertebral a. Atlas of Human Anatomy (7th ed.), Netter, F., Plate 150 11 https://link.springer.com/chapter/10.1007/978-3-319-67038-6_14 12 Medial medullary syndrome (Dejerine syndrome) Anterior spinal a. Disruption of Note: This lesion is unrelated to anterior Anterior spinal artery spinal artery syndrome in spinal cord Damaged structure Deficit Corticospinal tract (pyramid) Contralateral hemiparesis Medial lemniscus Contralateral loss of position sense, vibratory sense, and discriminative touch Hypoglossal nerve Deviation of the tongue to ipsilateral side when protruded; Bulbar Palsy - tongue atrophy and fasciculations Neuroanatomy through Clinical Cases (2 ed ed), Blumenfeld, Fig 14.8 13 Lateral medullary syndrome (Wallenburg syndrome) PICA Disruption of PICA or Vertebral Artery Damaged structure Deficit Spinothalamic tract Contralateral loss of pain and temperature sense on body Spinal trigeminal nucleus/tract of V Ipsilateral loss of pain and temperature sense on face Nucleus ambiguus Dysphagia, palate paralysis, hoarse voice, diminished gag reflex Descending hypothalamospinal tract Ipsilateral Horner syndrome (ptosis, miosis, anhidrosis, flushing of face) Vestibular nuclei (mainly inferior and medial) Nausea/vomiting, nystagmus, vertigo Inferior cerebellar peduncle/spinocerebellar fibers Ipsilateral ataxia Neuroanatomy through Clinical Cases (2 ed ed), Blumenfeld, Fig 14.8 14 Sympathetic NS Fibers from the hypothalamus travel close to the spinothalamic fibers in the lateral brainstem to reach the sympathetic cell column in the spinal cord T1-L2. Pre-ganglionic sympathetic neurons originate in the lateral horn of the spinal cord from T1-L2, enter the sympathetic trunk, then synapse in the superior cervical ganglion before entering the skull via the internal carotid arteries. Damage anywhere along this pathway could cause a “Central” Horner syndrome. Neuroanatomy through Clinical Cases (2 ed ed), Blumenfeld, Fig 13.10 15 Medial pontine syndrome Disruption of Paramedian branches of basilar a. Damaged structure Deficit Corticospinal tract Contralateral hemiparesis Medial lemniscus Contralateral loss of position sense, vibratory sense, and discriminative touch Abducens nucleus/PPRF Paralysis of conjugate gaze toward the side of the lesion (“wrong-way eyes”) Neuroanatomy through Clinical Cases (2 ed ed), Blumenfeld, Fig 14.19 16 Locked-in syndrome Occlusion of the basilar artery may result in a locked-in syndrome. Bilateral pons lesion, usually restricted to the basilar pons (damage to corticospinal and corticobulbar tracts). Typically, the only movement the patient will have is their eyes and eyelids. https://www.independent.co.uk/news/uk/home-news/locked-syndrome-sufferers-lose-legal-challenge-over-assisted-dying-8053451.html 17  Posturing in Coma Both postures characterized by extension and internal rotation of lower limbs, and plantarflexion Decorticate Posturing: Lesion above midbrain Flexion of arms wrist fingers Decerebrate Posturing: Lesion between Red Nucleus and Vestibular Nuclei Disinhibition of strong Lateral Vestibulospinal Reflex Not caudal to Vestibular Nuclei because disruption of vestibular nuclei will eliminate decerebrate posturing Opisthotonos(Gamma Rigidity) – extension adduction and hyperpronation of arms 18  Breathing Impedance Pneumography (IP) Patterns in Coma allows estimation of respiratory flow rates in comatose patients using skin electrodes placed Produced by lesions to Reticular around thorax Formation at different levels of the brainstem Hyperpnea – deeper than normal breathing (not necessarily faster) Deep Forebrain: Cheyne- Stokes Breathing Apnea – period of low/no airflow in or out Midbrain (and isthmus of pons): Central Neurogenic Hyperventilation 19  Rostral pons: Apneustic Breathing Apneusis – period of prolonged inspiration Mid-pons: Cluster Breathing (clusters of 3-4 followed by apneusis) Caudal Pons/Rostral Medulla: Ataxic Breathing (irregular spacing and depth) Mid-Medulla -> C5: Respiratory Arrest 20 Anencephaly (1:4600 births) Severe type of neural tube defect where some or all parts of forebrain fail to develop Presence of brainstem and cerebellum preserves normal “Primitive Reflexes” and responsiveness to auditory, vestibular, and painful stimuli (not visual stimuli) Child can move, suckle and even smile apparently normally Prognosis very bad, usually resulting in death within days after birth 21 Brainstem and Death Brainstem provides unconscious control of Medical death is not the death of all the body’s basic life functions like breathing, heartbeat, cells ( bone and skin cells can survive 70+ hours blood pressure, swallowing after “death”) Traditionally death was defined by the lack of Loss of forebrain function (either temporarily basic functions like breathing and heart beat or permanently) with a functional brainstem will produce a Vegetative State Modern technology (respirators, ECMO) allow for survival of patients even after cessation of In a vegetative state a patient can show sleep- independent heartbeat and respiration. wake cycles (unlike coma), movements such as grinding teeth, swallowing, crying, smiling, grasping another's hand, grunting or groaning Since ~1960s many medical and legal definitions and are responsive to loud sounds of death are now based on concept of Brain Death (aka Brainstem Death) For non-traumatic brain injuries the chances of recovery after 6 months are extremely low 22 23