Neurology — Short Cases

11 | Neurology—Short Cases Shu-Leong Ho, Raymond Tak-Fai Cheung, Windsor Mak, Kay-Cheong Teo, and Koon-Ho Chan Overview Elucidate the location and nature of the lesion in the nervous system. Assessing higher mental functions and discovery of any cranial nerve deficits, pyramidal, cerebellar, extrapyramidal signs or sensory disturbances can all help to locate the lesion. Age of the patient, timing and mode of onset, pattern of progres- sion, and response to empirical treatment may help to indicate the nature of the lesion. Examination of higher mental function Assess mood, attention, orientation, language, memory (short- term and long-term memory), calculation, abstract thought, spatial, and visual perception. Check orientation in time, place, and person. Assess for comprehension, expression, and repetition. For comprehension of language, ask patient to follow simple written or verbal commands, e.g., close your eyes, lift up your left arm. For expression of language, ask patient to name objects. Suggestions may be given if there is difficulty. For repetition, ask patient to repeat a phrase.

Neurology 143 Ask patient to repeat three objects such as apple, table, and penny, and then after 5 minutes ask for recall of the same objects (short-term memory). Ask patient to recall their telephone number, home address, distant events or names of famous persons (long-term memory). To test for calculation, ask patient to subtract 7 from 100, and 7 from the results thereafter. Ask patient to copy 2 intersecting pentagons; write the numbers on a round clock-face and draw the hands for a given time. Ask patient to name the number drawn on the palm of either hand or recognize coins of various denominations placed in either hand. To test for sensory inattention, touch the patient on each upper limb individually and simultaneously, with the patient’s eyes open and closed. Ask patient to name the side of the upper limb being touched. After ensuring that there is no visual field loss, test for visual inattention by asking patient to point to your finger which moves on either side of his visual field. Give a scenario to the patient and assess if there are any irra- tional or concrete thoughts. Ask patient the meaning of various proverbs. Ask patient for similarities between different objects with the same utility (e.g., boat and car, banana and apple). Examination of cranial nerves . Ask for loss of smell or taste. Inspect for scars, facial asymmetry, deformities, pupil size, proptosis. Check visual acuity of each eye using Snellen chart. If the patient is unable to see the chart, use finger counting, hand movement, and light from a torch. Compare the visual field of each eye on direct confrontation. Check direct and consensual pupillary responses, and test for the accommodation reflex by looking at a distant object fol- lowed by a near object. Look at both fundi.

144 Problem-Based Medical Case Management Examine eye movements for dysconjugate gaze and nystagmus (horizontal or vertical). Ask patient to bite and open the mouth against resistance. Perform the jaw reflex. Check for facial sensation. Use a clean cotton wool to examine for corneal reflexes. Ask patient to close both eyes tightly and look upwards (look for asymmetry of the forehead skin creases), show teeth and blow up the cheeks. Perform the Weber’s and Rinne’s test on both ears using a tuning fork (256 Hz). Listen for dysarthria, and test articulation by asking the patient to repeat standard words (e.g., British constitution, baby hip- popotamus) or sentences. Look for uvula movement and deviation, when the patient is asked to say “ahhh”. Perform the gag reflex. Inspect the relaxed tongue for muscle bulk and fasciculation. Ask patient to protrude the tongue, move the tongue from side to side or in/out, and protrude it into either cheek. Examination of limbs Observe: gait (during usual walking and if appropriate heel-toe walking), posture, muscle bulk, fasciculations, spontaneous or involuntary movements. Examine tone with the patient completely relaxed. Test strength of specific groups of muscles across single joints. Elicit limb reflexes with a tendon hammer, with the patient completely relaxed. If the reflex is absent or diminished, ask the patient to perform Jendrassik manoeuvres for reinforcement (e.g., clenching the teeth, interlocking of fingers in a hook-like form). If the reflex is brisk, test for clonus. Using the tendon hammer requires a lot of practice. The best effect comes from a wrist action to swing the hammer.

Case 11.1 Neurology 145 Elicit for plantar response. Assess for sensory deficits from two perspectives: — Modality (i.e., dorsal column or spinothalamic loss). — Distribution (dermatomal or glove/stocking loss). Test for bradykinesia and cerebellar signs if indicated. 11.1 Cerebellar syndrome Classical signs Truncal ataxia or limb ataxia with wide-based ataxic gait; unable to perform heel-toe walking despite normal strength Nystagmus on horizontal or vertical conjugate gaze Dysarthria, typically slow and slurred speech Intention tremor Past-pointing Dysdiadochokinesia Additional signs may be evident depending on the cause of the cerebellar syndrome, e.g., upper motor neuron signs in multiple sclerosis, wasting/lymphadenopathy/clubbing in paraneoplastic syndrome. Causes Cerebellar degeneration: idiopathic, paraneoplastic, familial Toxins and drugs: alcohol, anticonvulsants Cerebellar infarct, haemorrhage, tumour (primary or metastases) Important investigations Computed tomography/magnetic resonance imaging of brain Serum for paraneoplastic anti-neuronal autoantibodies * Cerebrospinal fluid analysis to exclude infection and inflammation

146 Problem-Based Medical Case Management Case 11.2 Discussion Neurological features may precede detection of malignancy. Common associated malignancies are carcinoma of lung, breast, and female genital tract. Pitfalls and tips Exclude muscle weakness before assessing for ataxia. In the presence of significant limb weakness, intention tremor and past pointing are difficult to interpret. Sensory ataxia typically worsens with eyes closed (positive Romberg’s test): 11.2 Chronic inflammatory demyelinating polyneuropathy (CIDP) Classical signs Progression over 8 weeks Symmetrical flaccid tone, proximal and distal muscle wasting, and weakness in all the limbs May develop foot-drop in more severe cases Diminished or absent limb reflexes May have absent plantar response Glove and stocking pattern of sensory loss Additional signs of iatrogenic complications: Cushingoid features because of long-term corticosteroid therapy, surgical scar posterior to lateral malleolus after sural nerve biopsy for diagnosis Cause . Immune-mediated demyelination of the peripheral nerves [

P Case 11.2 Neurology 147 Important differential diagnoses Diabetic distal symmetric sensorimotor polyneuropathy Acute or subacute forms of Guillain-Barre syndrome Hereditary motor sensory neuropathies (Charcot-Marie-Tooth disease), hereditary neuropathy with liability to pressure palsies (HNPP) Paraproteinemic or paraneoplastic neuropathies Neuropathies associated with connective tissue diseases Drugs or toxins (mercury, arsenic, N-hexanes, chloroquine, amiodarone, vincristine) Vitamin B12 deficiency HIV- or CM V-associated inflammatory neuropathy Important investigations Electrophysiological studies Cerebrospinal fluid analysis (elevated protein level but no pleocytosis) Screen for paraproteins, autoimmune connective tissue dis- eases, malignancies. Sural nerve biopsy (reduction in myelinated fibres, endoneurial mononuclear cell infiltration, onion bulb formation and other remyelinating features) Discussion Differential diagnosis and investigations of peripheral neuropa- thies. CIDP has a protracted course (over 8 weeks), progressive or relapsing-remitting in nature. Treatment: corticosteroids, immunosuppressants, intravenous immunoglobulins, plasmapharesis Pitfalls and tips Look for generalized and symmetrical ngture of the signs in the limbs.

148 Problem-Based Medical Case Management Case 11.3 Pes cavus indicates an earlier. pathogenic onset, developing in childhood (e.g., inherited causes) and is not present in late- onset neuropathies. Respiratory and bulbar muscles may be involved in advanced cases. 11.3 Lateral medullary syndrome Classical signs Ipsilateral signs: — Dysphagia, hoarseness of voice due to vocal cord paralysis, loss of gag reflex, soft palate paralysis, with uvula deviation when patient says “ahhh” (IX, X nucleus) — Horner’s syndrome (descending sympathetic fibres) — Loss of all sensory modalities of face (descending sensory tract and nucleus of V nerve) — Cerebellar ataxia with nystagmus towards the side of lesion (inferior cerebellar peduncle and cerebellar connections) Contralateral loss of pain and temperature sensation below the face Additional signs depending on cause: risk factors of stroke (e.g., xanthelasma, corneal arcus, nicotine stains, hypertension, diabetic features), recent neck trauma Causes Usually brainstem infarction from local thrombotic occlusion, arterial thromboembolism (e.g., vertebral artery dissection) or cardioembolism Brainstem haemorrhage Acute brainstem demyelination: multiple sclerosis Leukoencephalopathy with brainstem involvement (hyperten- sion, drugs, autoimmune diseases)

Case 11.3 Neurology 149 Important differential diagnoses + Acute vestibular neuronitis or benign positional vertigo, in which focal neurological signs (except for nystagmus) are absent Important investigations «+ Computed tomography/magnetic resonance imaging of brain + Exclude vascular risk factors Discussion + Most cases are due to occlusion of the vertebral artery and its lateral medullary penetrating arteries. Posterior inferior cer- ebellar artery occlusion accounts for < 15% of cases. Hence, cerebellar infarction is uncommon in this syndrome. The cer- ebellar signs are due to lesion affecting the inferior cerebellar peduncle and its connections in the brainstem. * Anti-platelet therapy remains the primary treatment for ischaemic stroke. The use of anti-coagulation is controversial in arterial dissection but 3 to 6 months of anti-coagulation is sometimes prescribed, or if there is progression of thrombosis despite anti-platelet therapy. Reperfusion therapy in acute ischaemic stroke Pitfalls and tips * If patient has occipital headache and neck pain, consider verte- bral artery dissection. If contralateral weakness is present (indicating involvement of the corticospinal tract located more medially), it indicates a more extensive lesion, such as haemorrhage, demyelination, Or tumour,

150 Problem-Based Medical Case Management Case 11.4 11.4 Amyotrophic lateral sclerosis (ALS) Classical signs Thin, may be breathless from respiratory muscle weakness Muscle wasting (may be asymmetrical) with fasciculation and weakness in the limbs and tongue. Typically a mix of upper and lower motor neuron lesion signs. Depending on the pre- dominant lesion, reflexes may be brisk, normal, absent, and asymmetrical. Plantar responses may be upgoing, down-going or absent. Palatal paralysis and dysarthria with nasal speech (bulbar or pseudobulbar palsy). Eye movements are preserved with a normal range of horizontal and vertical gaze. Absence of sensory signs Important differential diagnoses Cervical myelopathy with multiple radiculopathy: presence of sensory deficits and other signs, e.g., Hoffman’s sign, inverted supinator jerks; tongue and bulbar muscles not affected Spinal muscular atrophy: differentiated from ALS by the absence of upper motor neuron signs, more benign clinical course, and electromyogram findings Motor predominant neuropathy: lower motor neuron lesion signs, with or without sensory features Poliomyelitis: fasciculation in the acute stage; wasting, possible contractures, and other lower motor neuron lesion signs in the chronic stage Muscular dystrophy: presenting with distal or asymmetrical wasting in specific muscle groups, typically the shoulder or calf muscles; no sensory deficit Polymyositis: muscle fasciculations and weakness without any sensory features, especially affecting the proximal muscles; early wasting unusual

Case 11.4 Neurology 151 - Benign fasciculation syndrome: persistent muscle fascicula- tions with no identified cause; diagnosis by exclusion. « Thyrotoxicosis: muscle wasting and fasciculation possible Important investigations + Electromyogram: chronic denervation and reinnervation with high amplitude motor unit action potentials. Spontaneous muscle activity consisting of positive sharp waves, fibrillations and complex repetitive discharges. *+ Sensory and motor nerve conduction parameters are normal in early stages, but compound motor action potential amplitude may be reduced in severely wasted muscles. + Serum creatine kinase level is usually normal or slightly raised. *+ Magnetic resonance imaging of the cervical spine to exclude cervical cord pathology Discussion * Subtypes: primary lateral sclerosis (mainly upper motor neuron deficits); progressive muscular atrophy (mainly lower motor neuron deficits); progressive bulbar palsy (bulbar with upper and lower motor neuron deficits) Prognosis: 50% die usually from respiratory failure or aspira- tion pneumonia within 3 years; 90% die within 5 years. Riluzole has a survival benefit of about 3 months. Palliative care, nutrition, e.g., naso-gastric or percutaneous gas- trostomy feeding Consider intermittent ventilatory assistance or long-term mechanical ventilation. Depression is frequent. Consider coun- selling, family and social support, and antidepressants. Pitfalls and tips Look for fasciculations with the muscles at rest. Tap the muscles gently if none are observed; avoid rushing to tap muscles without properly observing them first.

152 Problem-Based Medical Case Management Case 11.5 ¢ Ask the patient to open the mouth without protruding the tongue and inspect for fasciculation. A normal tongue, when protruded may appear “fasciculating”. 11.5 Multiple sclerosis Classical signs ¢ Optic neuritis: impaired visual acuity, afferent pupillary defect, with diminished direct and consensual pupillary response to light ¢ Internuclear ophthalmoplegia: dysconjugate gaze palsy which results in impaired adduction in the ipsilateral eye with nystag- mus in the contralateral abducting eye on horizontal gaze ¢ Spastic paraparesis: unsteady stiff gait, characterized by increased tone and associated weakness in both lower limbs. Typically, brisk knee and ankle reflexes are encountered and the Babinski’s sign is present bilaterally. Reduced sensation in all modalities in both lower limbs, particularly in association with a sensory level. » Cerebellar signs: dysarthria, intention tremor and past-pointing on finger-nose test. Impaired rapid repetitive motion of the hands and feet (dysdiadochokinesia). Important differential diagnosis » Neuromyelitis optica (NMO) e Central nervous system manifestation of rheumatological diseases Important investigations * Blood for NMO-IgG * Magnetic resonance imaging of brain, brainstem, and spinal cord show multiple demyelinating plaques, typically in the periven- tricular regions, corpus callosum, and centrum semiovale

Case 11.6 Neurology 153 « Lumbar puncture for cerebrospinal fluid analysis may show presence of oligoclonal bands. + Visual evoked response may be delayed. Discussion « Multiple sclerosis is a demyelinating disease of the central nervous system, which demonstrates lesion disseminated in time and location. Typically, it presents with relapsing-remit- ting symptoms, but other clinical patterns occur, e.g., primary (progression of disease from onset) or secondary progressive (initial relapsing-remitting followed by progression), or pro- aressive relapsing (progressive from onset and during the inter- vals between each relapse). * Treatment: pulsed IV corticosteroids for acute relapse, immu- nomodulatory drugs to modify the course of the disease (i. interferon beta; ii. oral agents: fingolimod, dimethyl fuma- rate, teriflunomide; iii. monoclonal antibodies: natalizumab) Pitfalls and tips * Examine the fundus in a darkened room. Look for the red reflex. Zoom in slowly with the fundoscope, and orientate by locating the optic disc first. Think of internuclear opthalmoplegia when nystagmus is found with dysconjugate gaze. Demyelination of the peripheral nervous system, by definition, is not multiple sclerosis. 11.6 Parkinson’s disease Classical signs * Stooped posture (flexed at the trunk), thin, masked (expres- sionless) facies, soft monotone voice, drooling of saliva, greasy facial skin, typically in elderly patient

154 Problem-Based Medical Case Management Case 11.6 Stiff, shuffling or festinant (increasing rapid small steps with centre of gravity shifted forward) gait, lacking arm swing Resting tremor, typically asymmetrical, “pill-rolling”, affecting the hands Cog-wheel rigidity more prominent in the limbs compared to the trunk Bradykinesia (slow in initiating movement), may “freeze” during walking or turning Positive glabellar tap sign (unreliable) Power, sensation, and deep tendon reflexes are preserved. Important differential diagnoses Multisystem atrophy (MSA): 2 clinical subtypes, i.e., parkin- sonism with i) predominant pyramidal features (MSA-P), or ii) with predominant cerebellar ataxia (MSA-C). Autonomic failure is an important feature and occurs early. Bilateral vocal cord palsy causing stridor may be life-threatening. Progressive supranuclear palsy: vertical gaze palsy (unable to look up or down), prominent dysarthria, truncal rigidity. These patients lack resting tremor. Lewy body dementia: parkinsonism with hallucinations and psychosis occur in early stages of the disease, and eventual dementia. Wilson’s disease: Kayser-Fleischer ring best seen under slit- lamp examination, younger age at onset; consanguineous parents, prominent dystonia and patient may develop limb con- tractures, psychosis and jaundice. Cerebral small vessel disease and normopressure hydrocepha- lus may cause parkinsonism affecting the lower limbs more than upper limbs. Benign essential tremor: bilateral postural tremor, worse when performing a task. These patients may have head titubation or dystonia, but without parkinsonian signs.

Case 11.7 Neurology 155 Iinportant investigations + Family and drug history (e.g., long-term neuroleptics, antihista- mines, and illicit drugs) « Copper studies, slit-lamp examination in patient with young age of onset + Magnetic resonance imaging of the brain if atypical features (e.g., early onset cerebellar, pyramidal or autonomic distur- bance or dementia) are present. Discussion + Pathology: degeneration of dopaminergic nigrostriatal neurons, resulting in progressive loss of dopamine supply. Associated with Lewy bodies. + Principles of drug treatment and their complications Pitfalls and tips * Examine for atypical features, e.g., gaze palsy, cerebellar and pyramidal signs, early dementia or psychotic features, promi- nent truncal rigidity, prominent autonomic failure to help differ- entiate other forms of parkinsonism from Parkinson’s disease. * A typical pill-rolling, resting tremor, and asymmetrical par- kinsonian features in the upper limbs are helpful indicators of Parkinson’s disease. * Ask the patient to walk. Reduced arm swing is an early sign for Parkinson’s disease and walking may “bring out” resting tremor. 11.7 Polymyositis/Dermatomyositis Classical signs * Symmetrical proximal limb and neck weakness, muscle tenderness

156 Problem-Based Medical Case Management Case 11.7 Muscle bulk is usually spared, especially in early stages. Sensation is intact. Dermatomyositis if the skin is involved; typically there is a purple heliotrope in a butterfly distribution over the cheeks and eyelids that blanches with pressure. Skin manifestations may precede muscle weakness. Additional signs: Cushingoid features from corticosteroid treat- ment, cachectic appearance, lymphadenopathy, radiotherapy marks in patients with underlying malignancy Important differential diagnoses Polymyalgia rheumatica, typically affects elderly women, and may be associated with temporal arteritis. However, polymyal- gia rheumatica and temporal arteritis are rare in Chinese. Limb girdle muscular dystrophy (associated with early wasting in shoulder or pelvic girdle muscles) Myasthenia gravis: weakness is typically fatiguable and involves the eyes. Patients with systemic lupus erythematosus can have rash and myositis, classically a photosensitive butterfly facial rash. Important investigations o Increased serum creatine kinase level Electromyography shows myopathic changes. Muscle biopsy shows scattered fibre necrosis and perivascular inflammatory infiltration. Discussion Associated underlying malignancy, e.g., cancers of ovaries, lung, pancreas, breast, gastrointestinal tract, nasopharynx and non-Hodgkin’s lymphoma. Malignancy may develop before muscle weakness. Often follows a relapsing-remitting course

Case 11.8 Neurology 157 « Treatment: corticosteroids, immunosuppressants (azathioprine and cyclophosphamide), and intravenous immunoglobulins may be useful. Pitfalls and tips * Proximal weakness manifests as difficulty in climbing stairs, standing up from a squatting position, and combing hair. 11.8 Dysphasia Classical signs * Broca (expressive) dysphasia: non-fluent speech with diffi- culty in finding appropriate words. Naming and repetition are impaired. Comprehension is relatively preserved. * Wernicke (receptive) dysphasia: fluent but inappropriate speech with neologism and paraphasia. Comprehension is impaired. * Additional signs: right hemiparesis and right homonymous visual field defect, which reflect the extent of the lesion. Important causes Ischemic stroke is the most common cause of dysphasia. Haemorrhagic stroke Dementia: Alzheimer’s disease, frontotemporal dementia Encephalitis: Herpes simplex encephalitis may present with dysphasia. Patient is usually febrile. Tumour affecting the relevant regions Important investigations Computed tomography/magnetic resonance imaging of brain Exclude vascular risk factors Electrocardiogram to look for atrial fibrillation Lumbar puncture for cerebrospinal fluid analysis if indicated

158 Problem-Based Medical Case Management Case 11.9 Discussion e Language areas in the brain and localization for different dysphasia Pitfalls and tips * Some patients with impaired comprehension may still be able to obey one-stage commands. Comprehension to two- or three- stage commands should be tested. e Naming of object may not be fully impaired in mild cases. Test naming as many objects as possible. » Language is a dominant hemisphere function, which is on the left hemisphere for 96% of right-handed and 70% of left- handed individuals. 11.9 Syringomyelia (syringobulbia) Classical signs » Clawing of fingers, scars, and ulcers on the hands; wasting and weakness of small hand muscles and ulnar aspects of forearms ° Absent upper limb reflexes (if anterior horn cells are affected) and brisk lower limb reflexes, bilateral Babinski’s signs (if cor- ticospinal tracts are affected) » Dissociated pain and temperature loss of pin-prick and tem- perature in the affected dermatomes of the upper limbs e No loss of propioception or vibration ¢ Additional signs depending on cause and severity: mild kyphoscoliosis, short neck, Charcot’s joints at the elbow, Horner’s syndrome if the sympathetic fibres at the lateral horn of T1 are involved In syringobulbia (the upper cervical cord and lower brainstem are involved), there may be diplopia and nystagmus (medial longitu- dinal bundle), weakness of sternomastoid and trapezius muscles

Case 11.9 Neurology 159 (XI nerve nuclei), bulbar palsy with soft palatal paralysis, dysar- thria, wasted fasciculating tongue (XI, XII nuclei). Causes e Usually associated with a foramen magnum lesion which causes an expansion of the central spinal canal, e.g., Arnold- Chiari malformation, hydrocephalus * Spina bifida, tumour, trauma, spinal arachnoiditis Discussion * It is a syndrome (with different causes) produced by a fluid- filled expanded syrinx arising from central spinal cord, typi- cally occurs in the cervical and upper thoracic cord. It affects decussating fibres of the spinothalamic tracts, anterior horns of the spinal segments, sympathetic fibres at C8/T1 (Horner’s syndrome). If the syrinx extends to involve the corticospinal tracts located more laterally, upper motor neurons lesion signs ensue in the lower limbs. Syringobulbia affects the medial lon- gitudinal bundle (nystagmus), descending trigeminal sensory nuclei (facial sensory loss), and XI, XII nuclei (weakness of sternomastoid and trapezius muscles, and bulbar palsy). * Surgical decompression of the syrinx, physiotherapy, occupa- tional therapy, other supportive care, and symptomatic measures Important investigations Magnetic resonance imaging of the cervical spine/brainstem Pitfulls and tips * Important to check for dissociated sensory loss in patients with bilateral wasted and atrophic hands

160 Problem-Based Medical Case Management Examination case Examination case scenarios i. Examine this hemiplegic patient’s upper limbs Important signs e Flexed posture at right elbow, with diminished spontaneous movement. Spasticity and weakness of right upper limb compared to the left. « Brisk biceps, supinator, and triceps reflexes on the right upper limb compared to the left. « Additional signs: drooling of saliva because of upper motor neuron facial palsy, lack of cortical signs. Diagnosis Cerebral infarction or haemorrhage at subcortical region Questions 1. What are the expected findings in the computed tomography of brain? e Infarction (hypodense lesion), haemorrhage (hyperdense lesion). 2. What are the common risk factors for a cerebral infarction? * Hypertension, diabetes mellitus, smoking, hyperlipidaemia, strong family history of strokes.

Examination case Neurology 161 ii. Examine the eyes of this man (visual field and fundoscopy are not required). Important signs » No chemosis or proptosis « Complete ptosis of right eye with a right dilated pupil, in a depressed and abducted position « Right efferent pupillary reflex defect, but the afferent responses are spared bilaterally + Dysconjugate eye movements; unable to adduct and look up with right eye Diagnosis Right complete III nerve palsy Question What is an important cause that you would need to exclude? + Unruptured aneurysm compression on the III nerve. Pitfalls and tips « In partial ptosis, consider Horner’s syndrome, myasthenia gravis, and partial I nerve palsy. The size and response of the pupils are helpful in helping to differentiate between myasthenia gravis, complete III nerve palsy, and Horner’s syndrome.

162 Problem-Based Medical Case Management Examination case iii. This 55-year-old man complained of progressive weakness, numbness and difficulty walking over the past month. Examine his lower limbs. Important signs * Symmetrical spasticity and weakness of both lower limbs * Brisk knee and ankle reflexes bilaterally, with clonus elicited in his right ankle « Bilateral Babinski’s sign ¢ Reduced sensation in all modalities in both lower limbs Diagnosis Spastic paraparesis Questions 1. What other examination would you specifically like to do? * Examine his upper limbs to exclude any abnormal signs, and look for a sensory level in his trunk. 2. Where is the most likely location of the neurological lesion, assuming that the upper limbs are normal? * Thoracic cord lesion. 3. This patient also complained of severe mid-back pain. He is a heavy smoker and was recently diagnosed to have lung carcinoma. What is a likely pathology? ¢ Thoracic cord compression from vertebral collapse caused by bony metastases.

Examination case Neurology 163 iv. This 50-year-old woman complained of facial weakness and drooling of saliva on her right side, over the past two days. She was recovering from an upper respiratory tract infection prior to developing these symptoms. Examine her face. Important signs « Asymmetrical loss of nasolabial folds on her right face + Right upper and lower facial weakness including right eyelid closure such that she is unable to close her right eye lid completely « Some increase in lacrimation from her right eye « Her eye movements, bulbar functions including her tongue and palate are spared. o There is no loss of facial sensation. Diagnosis Right lower motor neuron facial palsy (right facial nerve palsy) Questions 1. What other symptoms or signs might this woman have relating to your diagnosis? « Loss of taste and hyperacusis (sounds seem loud but distorted). 2. What is the most likely cause? * Bell’s palsy. 3. What other examination may reveal an important treatable cause? « Examination of her external auditory meatus and eardrum, to exclude Ramsay-Hunt syndrome and otitis media.