Presentation on theme: "CBL Review & CN Lesions Chad Byworth & Sean Botham."— Presentation transcript:
CBL Review & CN Lesions Chad Byworth & Sean Botham
You are the F1 on the receiving ward for James de Montfort, it is the morning ward round five days after his admission and the consultant has asked you to summarise the patient... This is James de Montfort, 32, admitted 5 days ago from the ED following a RTC. On admission he had loss of all sensory & motor function below T5 with an absent anal wink. He now has 3/5 power on the right lower limb, 1/5 power on the left lower limb with altered sensation on the right below T5 and normal anal wink. CT & MRI show a T4/5 vertebral fracture with cord oedema. These findings are consistent with a diagnosis of Brown-Séquard syndrome with spinal shock following cord hemisection at the T5 vertebral level.
What is Brown-Séquard Syndrome? A clinical syndrome where a hemicord lesion leads to: Ipsilateral UMN weakness below the lesion Ipsilateral loss of vibration & proprioception below the lesion Contralateral loss of pain & temperature sensation 1-2 dermatomes below the lesion What tracts cause the following symptoms? Describe their route... Ipsilateral UMN weakness Ipsilateral loss of vibration & proprioception Contralateral loss of pain & temperature
Ipsilateral UMN weakness Lateral Corticospinal Tract Originate in the cortex, pass through the internal capsule and then decussate at the pyramids at the lower margin of the medulla, travel down cord to synapse with ipsilateral LMNs. Ipsilateral loss of Vib & Pro Dorsal Columns 1 st order neurons travel ipsilaterally up cord to synapse. 2 nd order neurons decussate in the medulla and travel in medial lemniscus to thalamus. 3 rd order neurons travel from thalamus to cortex. Contralateral loss of Pain & T Spinothalamic Tract 1 st order neurons travel ipsilaterally 1-2 levels up cord to dorsal horn. 2 nd order neurons decussate in the cord and travel to thalamus. 3 rd order neurons travel from thalamus to cortex.
Describe the signs you would see in UMN lesions... Spastic Paralysis Hyper-reflexia Clonus No muscle wasting No fasciculations What is the prognosis in Brown-Séquard Syndrome? Prognosis for significant motor recovery in Brown Séquard syndrome is good. The majority of recovery occurs within the first 1-2 months following injury. It then slows but continues for 3-6 months. The most common pattern of recovery includes: Recovery of the ipsilateral proximal extensor muscles prior to that of the ipsilateral distal flexors Recovery from weakness in the extremity with sensory loss before recovery occurs in the opposite extremity Recovery of voluntary motor strength and a functional gait within 1-6 months
How does ipsilateral motor recovery occur? A small proportion (~ 10%) of motor fibres do not decussate in the pyramids and travel down the cord as the ventral (anterior) spinocortical tract. These then decussate at the level of the LMNs allowing the action potential to bypass the lateral spinocortical tract lesion. What are some potential long term complications of Brown-Séquard Syndrome? Complications can occur due to loss of motor, sensory and autonomic function. Common complications are: Pressure ulcers Pneumonia UTI DVT & PE Postoperative infection
What is spinal shock? Spinal shock is the transient absence of all voluntary and reflex neurological activity below the level of an acute spinal cord injury. It manifests as: Absent/reduced reflex Flaccid paralysis Loss of sensation It can last from days to months. How is this different from neurogenic shock? Neurogenic shock is a form of circulatory shock wherein the loss of sympathetic outflow below the level of a spinal injury leads to loss of vasomotor tone. This leads to hypotension and potentially bradycardia and an inability to regulate body temperature depending on the level of the injury. It can occur in any spinal injury above the T5 vertebral level.
A 7 year old school child was playing in the park when he knocked himself unconscious with a blow to the front of the head. In the ED he was found to have clear liquid running from his nose which had glucose ++ on dipstick. Imaging studies shows anterior cranial fossae trauma. He has no previous medical history. He has a full record of immunisations. What is the most likely diagnosis? A – Viral infection e.g. URTI. B – Meningioma within the olfactory groove C – Cribriform plate fracture leading to CSF rhinorrhea D – Diabetic neuropathy What is a risk of this injury? Retrograde infection from the nasal cavity into the meninges. Will his sense of smell return? No. Trauma tears free nerve endings passing through cribriform plate.
A 56 year old lady went to her GP for a 2 months history of headaches and more recently, seizures. Following a cranial nerve exam he found her left eye to be central and completely immobile and unable to open the eyelid, and sensation on the left side of her forehead was diminished. What is the most likely diagnosis? A – Meningioma compressing the left superior orbital fissure. B – Bleed from the internal carotid artery. C – Pituitary adenoma compressing the optic chiasm inferiorly. D – Epilepsy. What runs through the jugular foramen? IJV, CNs IX, X, XI Through what foramen does CN Vc pass? Foramen ovale.
A 46 year old gentleman goes to see his GP with an dry and itchy right eye, difficulty in smiling properly and reduced hearing acuity. Following a referral to the neurologists, imaging studies found an acoustic neuroma on the right side. Where, on this diagram, is the lesion likely to be? Facial Canal Stapedius Greater Petrosal Nerve Chorda tympani Internal Acoustic Meatus CNVIII CNVII Muscles of facial expression Stylo- mastoid foramen Parotid Gland Would the lesion be more proximal or more distal if he had presented with these symptoms and hyperacusis as well? Proximal. Hyperacusis indicates loss of innervation to stapedius.
A 73 year old gentleman came in for a routine carotidendoartarectomy. Following the procedure the surgical FY1 noticed muscle wasting in his tongue. When asked to stick out his tongue he was able to do so but it pushed towards the right side. The patient did not do this before the procedure. What happened? Severing of right hypoglossal nerve as it runs over the superficial and lateral aspect of ICA and ECA. Important: specify side! Or no mark for you.
As his wife visits him, the reg notices that she smiles unusually. Being the caring reg he is he investigates further, and diagnoses an upper motor neuron lesion of the right facial nerve. What would the pattern of injury be and why? Forehead part of facial nerve nucleus has bilateral UMN innervation whilst lower face only has contralateral UMN innervation. An UMN lesion will paralyze contralateral lower face but forehead will be okay due to its bilateral supply. What simple movement can you ask a patient to perform to tell if the lesion is upper or lower motor neuron? Wrinkle their forehead. If they can = UMN, if they can’t = LMN.