137 Chapter 9 Neurology presenting syndromes Altered consciousness 138 Headache 139 SUBASH KC/NMC-15TH/2014 138 CHAPTER 9 Neurology presenting syndromes Altered consciousness Measured on the Glasgow Coma Scale, this can vary from mild confusion to coma. Clues are often in the history to determine the cause, e.g. trauma/infective/ toxic. Imaging may be urgently needed to identify surgically treatable causes, e.g. extradu ral hemorrhage in trauma patients. \200 Infection: Meningitis: bacterial/viral. \200 Encephalitis. \200 Empyema. \200 Intracerebral absc ess. Hemorrhage (traumatic or spontaneous rupture, e.g. AVM): Intra-axial: within the brain parenchyma. \200 Extra-axial: outside the parenchyma. Ischaemic: Cardiorespiratory arrest. \200 Near drowning. \200 Hypovolaemia (important in trauma pa tients). Toxic: Carbon monoxide poisoning. \200 Overdose, e.g. heroin. Metabolic: Diabetic ketoacidosis. \200 Hepatic encephalopathy. \200 Renal failure. \200 Metaboli c disorders. Tumor. \200 Epilepsy (post ictal). \200 Vascular: Stroke. Demyelination disorders. Role of imaging CT Useful in the acute setting, to exclude hemorrhage, space-occupying lesi ons, identify stroke, or evidence of established ischaemia. SUBASH KC/NMC-15TH/2014 HEADACHE 139 Headache The majority of patients with headaches do not require imaging. Worrying symptoms include signs of increased intracranial pressure such as head- aches worsening on lying \202 at, bending down, or worsening daily head- aches should be investigated. Headaches pre senting acutely associated with meningism should be investigated immediately. \200 Infect ion: Meningitis. \200 Encephalitis. \200 Sinusitis. \200 Hemorrhage: Subarachnoid, intracerebral, or extra-axial. Post-traumatic. \200 Raised intracranial pressure: Brain tumors. \200 Idiopathic intracranial hypertension. Venous sinus thrombosis. Role of imaging CT Useful in acute presentation, urgently if associated with meningism. SUBASH KC/NMC-15TH/2014 This page intentionally left blank SUBASH KC/NMC-15TH/2014 141 Chapter 10 Neurology conditions Stroke 142 Subarachnoid hemorrhage Subdural hemorrhage 146 Encephalitis 148 Brain abscess 1 50 Hydrocephalus Acoustic neuroma Glioma 156 Meningioma 158 Brain metastases 160 Pituitary adenoma 162 Multiple sclerosis 164 Epilepsy 166 144 152 154 SUBASH KC/NMC-15TH/2014 142 CHAPTER 10 Neurology conditions Stroke Stroke is an acute episode of neurological de \201 cit. Transient ischaemic attacks (TIAs) are neurological events that resolve within 24 hours (usually within 1 \200\2232 ho urs). Stroke is a major health problem in the UK accounting for 11 % of annual deaths as we ll as signi \201 cant morbidity. Causes \200 80 % thrombotic (cerebral infarction). \200 15 % haemorrhagic. \200 5 % n on-traumatic subarachnoid hemorrhage (SAH). \200 1 % venous occlusion. Clinical presentation Patients present with facial and limb weakness, slurred speech, numbn ess, blurred vision, confusion and headache. FAST ( used to rapidly screen patients. F ace A rm S peech T est) is 110,000 people will suffer a \201 rst or recurrent stroke every year in England. Thrombol ytic therapy is indicated for use in thrombotic stroke. This must be given within 3 hours o f onset of symptoms once hemorrhage has been excluded. Realistically this will be within 6 hours of symptom onset within a specialized stroke unit. Imaging Ultrasound Doppler ultrasound of the carotid arteries is used in patients with TIA or non-disabling stroke as part of the work-up for possible carotid endarter- ectomy. Carot id artery stenosis is calculated from assessing arterial \202 ow rates. Symptomatic patie nts with stenoses > 70 % are considered candi- dates for endarterectomy. CT (Fig. All patients with a suspected stroke should have a non-contrast CT (NCCT) of the b rain within 24 hours. Immediate imaging (within 1 hour) is indicated in the following circu mstances: \200 Indications for thrombolysis or early anticoagulation treatment. \200 An ticoagulant treatment. \200 Known bleeding tendency. \200 Glasgow Coma Score (GCS) <13. \200 Unexplained progressive or \202 uctuating symptoms. \200 Papilloedema, neck sti ffness, or fever. \200 Severe headache at symptom onset. 10.1 ) NCCT is used to exclude hemorrhage or other causes. Early NCCT in stroke is often normal. I nitial \201 ndings include loss of gray/white differen- tiation, sulcal effacement, and a hyperdense (bright) clot within a major cerebral artery (the hyperdense MCA sign). Later, within 12 \200\22324 hours, oedema can be detected as low density within the brain parenchy ma. Old/ mature infarcts are hypodense (dark) on NCCT and associated with local atrophy. SUBASH KC/NMC-15TH/2014 STROKE 143 MRI is more sensitive than CT in detecting oedema \200\224 within 6 hours, but is not as widely available in the acute setting. Oedema is seen as high signal on T2 an d FLAIR imaging. Intracerebral hemorrhage is seen as a high density (bright) focus on NCCT. This most often occurs secondary to hypertension, 80 % are within the basal ganglia. The MRI appearance of hemorrhage differs according to the age of the blood products. Various other techniques can be used in the imaging of stroke. These include: CTA, CT/MR pe rfusion studies, and diffusion weighted MRI. These will be used in specialist stroke center s and are not yet widely used in acute stroke imaging. Information for the radiologist An accurate history is vital to assess whether the patient is a candidate for thrombolysis or any of the other indications for immediate imaging (see earlier in section). What are the patient \200\231s current clinical state and GCS? Patients who are confused can be uncooperative and dif \201 cult to scan. Patients with a low GCS may have dif \201 culty protecting their airway and anesthetic support may be required prior to sca nning. Patients with known malignancy may have intracranial metastases causing their symptoms. The se are not always visible on NCCT and therefore a contrast enhanced CT scan may be indicate d. (a) (b) Fig. 10.1 arrow shows an area of low attenuation. b) Axial T2 MRI showing the full extent o f the stroke. A 77-year-old male with left visual disturbance. a) Axial CT image, the SUBASH KC/NMC-15TH/2014 144 CHAPTER 10 Neurology conditions Subarachnoid hemorrhage SAH is the presence of blood within the subarachnoid space, which c an sometimes extend into the intraventricular space. Vasospasm and cerebral infarction is t he leading cause of death in SAH. Causes \200 Rupture of cerebral aneurysm (90 \200 Trauma. \200 Arteriovenous malforma tion (AVM). \200 Coagulopathy. \200 Extension of intracerebral hemorrhage. \200 Idiop athic (5 % ). % ). Clinical presentation Headache \200\224 sudden onset, worst ever, \200\230thunderclap \200\231, often radiating towards occiput. Neck stiffness and photophobia related to mening eal irritation by blood products are often present. Nausea, vomiting, confu- sion and decre ased level of consciousness are symptoms related to raised intracranial pressure. Patients may present with symptoms related to complications such as hydrocephalus, vasospasm, and st roke. Patients with a history of polycystic kidney disease, aortic coarctation, \201 bromuscula r dysplasia, and collagen vascular disorders are at increased risk of cerebral aneurysm. Imaging NCCT is the mainstay of diagnosis (Fig. \201 rst 24 hours. High-density (bright) blood can be seen in the basal cis- terns, Sylvian \201 ssure, ventricles, over the corti cal sulci, or interhemispheric \201 ssure. The site of the blood can point to the locatio n of the ruptured aneurysm. 10.2 ). It is sensitive (95 % ) in the Hydrocephalus is an early complication and can be detected on CT as dilatation of the ventricles. MRI is more sensitive than CT in detecting SAH in the subacute phase (after 48 hours) and c hronic SAH. If imaging is negative then lumbar puncture is required to con \201 rm the dia gnosis. Further imaging is directed at identifying the underlying cause. CTA is as accurate in diag nosing cerebral aneurysms as standard catheter angio- graphy. This is readily available in most centers, is non-invasive, and can be performed immediately following the diagnostic NC CT. Most cerebral aneurysms can be treated endovascularly by the placement of coils. Information for the radiologist The patient \200\231s clinical condition and GCS is importa nt. Anesthetic support may be required. SUBASH KC/NMC-15TH/2014 SUBARACHNOID hemorrhage 145 Fig. 10.2 Axial non-contrast-enhanced CT image showing extensive subarachnoid hemorrhage (t he central white areas). SUBASH KC/NMC-15TH/2014 146 CHAPTER 10 Neurology conditions Subdural hemorrhage Subdural hemorrhage (SDH) is the presence of blood within the subdural space. These are usually secondary to tears in the emissary veins as they cross the subdura l space. Acute SDHs have a high associated mortality due to the fact that they are usually secondary to high-energy acceleration/deceleration mechanisms with a high incidence of other injuries. They can cause an increase in the intracranial pressure with brain tissue injury being the result. Predisposing factors include: Alcohol dependence. \200 Elderly. \200 Infants. \200 Anticoagulants. \200 Idiopathi c (5 % ). Clinical presentation These fall into 2 distinct types: \200 Acute: these usually present with a headache and a decreasing level of consciousness. There is usually a good preceding history of trauma. \200 Chronic: these a re more insidious in nature and can develop over weeks. The initial injury may be relatively minor. As these develop over a long timescale t his means that there is a far greater opportunity to successfully treat these once diagnose d. Imaging (Fig. NCCT is the investigation of choice due to its availability. Blood is usually seen in a crescentic con \201 guration adjacent to the skull. Unlike SAHs the blood isn \200\231t restricted by the suture lines and can extend over a full hemi-sphere. 10.3 ) Chronic bleeds can be more problematical in that the blood can be the same density as the brain. This can make identi \201 cation of these very dif \201 cult. MRI is more sensitive than CT at delineating the extent of chronic subdural haematomas as w ell as underlying brain tissue injury. In addition MRI is far more sensitive at identifying small and isodense haematomas. Information for the radiologist The patient \200\231s clinical condition and GCS are import ant. Anesthetic support may be required. SUBASH KC/NMC-15TH/2014 SUBDURAL hemorrhage 147 Fig. 10.3 the past week and sudden onset of headache 4 hours ago. The 2 arrows point to sub dural hemorrhage. The anterior bleed is bright consistent with an acute bleed and the poste rior bleed is isodense with the adjacent brain tissue consistent with a 1-week-old bleed. N otice also the ventricular effacement on the right and loss of the gray-white differentiati on consistent with raised intracranial pressure. Axial CT head image of a patient with steadily deteriorating gait over SUBASH KC/NMC-15TH/2014 148 CHAPTER 10 Neurology conditions Encephalitis Encephalitis is de \201 ned as in \202 ammation of the brain parenchyma. It is usually secondary to viral infection, but can also develop secondary to bacterial and fu ngal meningitis. The most common cause of fatal encephalitis in the UK is herpes simplex vi rus (HSV-1). HSV-2 causes congenital encephalitis in neonates. Acute disseminated encephalomyelitis (ADE M) is an immune response to viral infection or less commonly vaccination. It is more common in children. Clinical presentation Many encephalitides are mild and self-limiting. Only a minority will develop into a serious illness. Headaches, fever, mood changes, and drowsiness are initial presenting signs and symptoms. Focal neurological signs, seizures, coma, and death or lasti ng brain injury follow. ADEM is clinically similar to viral encephalitis, but usually recovers within 2 \200\2233 weeks, although 10 \200\22320 damage. % of patients suffer long-term brain Imaging CT (Fig. Subtle oedema, in the temporal lobes and adjacent posterior frontal region s with local mass effect can be seen on NCCT in the \201 rst 2 \200\2233 days. 10.4 ) These minimal changes are in contrast to marked clinical impairment. Hemorrhage may give rise to areas of patchy increased density. Enhance- ment following IV c ontrast is common. MRI Gyral oedema is seen as low signal (dark) on T1- and high signal (bright) on T2-weighte d and FLAIR sequences. MRI is more sensitive to white matter changes than CT and will demon strate them both earlier and their full extent. Hemorrhage may be visible as high signal on T1 and signal voids on T2 lowing IV gadolinium will be similar to that seen on CT. imaging \200\224 these changes imply necrosis. Enhancement fol- Information for the radiologist The clinical condition of the patient is important. As stat ed earlier, CT changes may be minimal in a seriously ill patient and may warrant an early M RI. If the patient has a depressed level of consciousness anesthetic support may be require d, see b OHCM , pp. 400 and 834. SUBASH KC/NMC-15TH/2014 ENCEPHALITIS 149 Fig. 10.4 (arrows) consistent with herpes simplex encephalitis. Axial CT image showing low attenuation areas on both temporal lobes SUBASH KC/NMC-15TH/2014 150 CHAPTER 10 Neurology conditions Brain abscess Brain abscess is a focal infection (usually bacterial) that behaves like an e xpanding mass. Typical causes are Streptococcus milleri , Staphylococcus , tuberculosis, fu ngal, or parasitic infection. Multiple abscesses are seen in immunocompromised patients suc h as those with HIV/AIDS or following organ transplant. Intravenous drug users (IVDU) are a t increased risk. Bacteroides , Clinical presentation \200 Headache and focal signs, depending on the location of the abs cess are typical. Seizures and signs of raised intracranial pressure such as vomiting are common. Fever and elevated white cell count, CRP, and ESR are usual. The duration of clinical symptoms is variable, but cerebellar abscesses may progress rapidl y due to hydrocephalus. Imaging CT NCCT will demonstrate low-density area/s. These typically show ring enhancement following IV contrast (Fig. the breakdown of the blood \200\223brain barrier in the abscess capsule. Other features include surrounding vasogenic oedema (low density) and mass effect such as sulcal effacement and shift of the midline structures. 10.5 ). The enhancement is due to Hydrocephalus can be seen in association with posterior fossa abscesses. Enhancement of the ventricular lining (ventriculitis) implies intraventricular extension of the abscess, whic h carries a poorer prognosis. MRI On MRI the necrotic abscess center and surrounding brain oedema will appear hyperintens e (bright), similar to CSF, on T2-weighted and FLAIR imaging. The abscess capsule enhances following IV gadolinium on T1-weighted imaging. Information for the radiologist Neurological status and GCS will help the radiologist to pr ioritize investiga- tions. Patients with decreased levels of consciousness, seizures, or fo cal neuro- logical de \201 cits require urgent imaging. Patients with depressed consciousn ess may require anesthetic support. Further information such as whether the patient is immunocompromised or an IVDU is very helpful. SUBASH KC/NMC-15TH/2014 BRAIN ABSCESS 151 Fig. 10.5 Axial CT showing multiple ring-enhancing lesions within the brain, with signi \201 cant amount of perilesional oedema, and midline shift in a patient with multifocal abs cesses. SUBASH KC/NMC-15TH/2014 152 CHAPTER 10 Neurology conditions Hydrocephalus Hydrocephalus is an imbalance in the production, \202 ow, and absorption of cerebrospinal \202 uid (CSF) leading to a rise in interventricular pressure. \200 Comm unicating hydrocephalus occurs when there is either over production of CSF, defective absorption, or venous drainage insuf \201 ciency, but there r emains open communication between the ventricles and subarachnoid space, e.g. following men ingitis or SAH. Non-communicating hydrocephalus occurs when there is obstruction to CSF \202 ow either between the ventricles or between the ventricular out \202 ow and the subarachnoid space. This is most commonly caused by either a congenital abnormality or by an intracranial tumor. Stenosis of the aqueduct of Sylvius connecting the 3 most common site of congenital obstruction. rd and 4 th ventricles is the Clinical presentation In adults the most common presentation is of cognitive decline. Other symptoms include headache that is often worst in the morning, nausea, vomiting, and visual disturbance. In children symptoms may be non-speci \201 c and include irritability, drows iness, poor feeding, and headaches. Imaging Plain \201 lm In babies and infants there will be bulging of the anterior fontane lle, and widening of the sutures. Ultrasound May be used in infants in whom the anterior fontanelle is still patent to assess the size of the ventricles. It is particularly useful in assessing for subependymal and in traventricular hemorrhage, which may lead to hydrocephalus. CT There will be enlargement of the ventricles, with rounding of the frontal horn shape and corresponding dilatation of the temporal horns with the lateral ventricles (Fig. 10.6 ). T here will often be periventricular low-density indicating transependymal \202 ow of CSF. The most important distinction to make is between hydrocephalus and white matter atrophy. P revious imaging may be very useful in making this distinction. MRI The same criteria are used for diagnosing hydrocephalus on MR as on CT. Transependymal CSF \202 ow is best appreciated as high signal on FLAIR sequences. Information for the radiologist Any previous imaging of the brain is crucial in interpretin g the presence or progression of hydrocephalus. SUBASH KC/NMC-15TH/2014 HYDROCEPHALUS 153 Fig. 10.6 Axial non-contrast-enhanced CT image showing gross dilatation of the ventricles. In addition there is effacement of the sulci. These \201 ndings are consistent with hydro cephalus. SUBASH KC/NMC-15TH/2014 154 CHAPTER 10 Neurology conditions Acoustic neuroma Otherwise known as a vestibular schwannoma. This is a benign intracranial, extra-axial tumor, which arises from the myelin cells of the vestibulococh- lear nerve (CN VIII). In 85 % they arise from the vestibular portion and in 15 % from the cochlear portio n. The most common location is the internal audi- tory canal but they may also arise at the cerebellopontine angle. Associations Acoustic neuromas may occur sporadically or as part of von Recklinghausen \200 \231s neuro \201 bromatosis. \200 In neuro \201 bromatosis type I a schwannoma may spor adically involve the VIII th nerve. Bilateral acoustic neuromas are rare. In neuro \201 bromatosis type II bilateral acoustic neuromas are almost pathognomonic. They tend to present below the age of 21. Clinical presentation There is usually a long, progressive history of sensorineural hearing loss and most patients also complain of tinnitus. Other symptoms include pain, vertigo, an d ataxia. Larger tumors may start to cause symptoms associ- ated with raised intracranial p ressure such as nausea, vomiting, headache, and eventually a decreased conscious level. Imaging Plain \201 lm There may rarely be erosion of the internal auditory canal. CT These usually present as an isodense tumor, on non-enhanced CT, which enhances uniformly following IV contrast. There is no internal calci \201 cation within the tumor. CT will d etect almost all tumors not so sensitive for very small lesions. > 2cm in size but it is MRI They are usually darker than brain tissue on T1 and show intense enhance- ment followin g IV gadolinium (Fig. 10.7 ). On T2 imaging the tumor will appear bright. Angiography The vascular supply is usually from the external carotid artery. Displacement o f the nearby vessels is the most common \201 nding at angiography. Information for the radiologist \200 Does the patient have any other stigmata of neuro \201 bromatosis, e.g. multiple neuromas, caf au lait spots, or axillary freckling? Are the symptoms unilateral or bilateral? SUBASH KC/NMC-15TH/2014 ACOUSTIC NEUROMA 155 (a) (b) Fig. 10.7 images. The arrow shows the normal right vestibulocochlear nerve with no evidence of enhancement. The arrowhead shows the abnormal nerve on the other side with marked enlar gement and signi \201 cant enhancement. a) Coronal image. b) Axial image, both are T1-weighted post-gadolinium SUBASH KC/NMC-15TH/2014 156 CHAPTER 10 Neurology conditions Glioma Glioma describes a tumor, which arises from the glial cells. The most common locatio n is the brain, but they also occur in the brainstem, the spinal cord, and the optic nerve. The tumors are further classi \201 ed according to cell of origin, location, and by grade . Classi \201 cation Cell of origin \200 Astrocyte: astrocytoma. Glioblastoma multiforme i s the most common type of astrocytoma. These are very aggressive. Ependyma: ependymoma. \200 Oligodendrocyte: oligodendroglioma. \200 Medulloblast: medul loblastoma. Location Gliomas may be supratentorial or infratentorial. In adults they are mostly suprate ntorial and in children mostly infratentorial. Grade \200 Low grade: these tend to be slow growing benign and carry a better prognosis. High grade: tend to be more aggressive, malignant, and carry a worse prognosis. Clinical presentation This will depend upon the area affected. Brain gliomas cause signs an d symptoms associated with raised intracranial pressure such as headache, nausea, vomiting, decreased conscious level, as well as seizures and cranial nerve palsies. Generalized symp toms such as memory loss and personality change are also common. A glioma originating in the spinal cord may manifest with weakness and paraesthesia in the limbs or with pain in the spine. Imaging CT On NCCT gliomas appears as an irregular and poorly de \201 ned low-density area causing mass effect. There will usually be enhancement following IV contrast but the patte rn is variable and non-speci \201 c. MRI (Fig. Tumors are typically low signal on T1 imaging and high signal on T2 imaging, usua lly with surrounding oedema. They enhance following gadolinium. 10.8 ) Angiography Whilst this technique is unlikely to be used for diagnostic purposes, it may be performed prior to surgical intervention and will often show an extremely irregular vascul ar pattern. Information for the radiologist \200 Focal neurological signs. \200 Are there any signs of cord compression or raised intracranial pressure? SUBASH KC/NMC-15TH/2014 GLIOMA 157 (a) (b) Fig. 10.8 A 25-year-old patient was referred for MRI as they had severe intractable headach e with vomiting. a) T2W axial image which shows extensive oedema with a more complex centra l abnormality in the right. b) T1W Gd axial image showing marked enhancement of the lesion. This was proven to be an astrocytoma. SUBASH KC/NMC-15TH/2014 158 CHAPTER 10 Neurology conditions Meningioma This is the most common extra-axial tumor in adults. Although usually a benign t umor it can, rarely, undergo malignant transformation. It arises from the meninges and is u sually supratentorial in location (90 usually slow growing but may be surgically resected i f causing signi \201 cant symptoms. % ). They are The peak age incidence is 45 years and they are relatively rare in children. There is no known cause but risk factors include: Neuro \201 bromatosis type 2. \200 Radiation to the head and neck. \200 Exposure to fe male hormones and breast cancer. Clinical presentation Symptoms are caused either by direct pressure on underlying brain par enchyma, raised intracranial pressure, involvement of cranial nerves, or involvement of sur rounding bone and soft tissues. These include non- speci \201 c headaches, seizures, focal weakness, and cranial nerve palsies. However, many are asymptomatic and are purely inciden tal \201 ndings. Imaging Plain \201 lm The most common \201 nding on a plain radiograph would be hyperos tosis of the bone adjacent to the meningioma. Calci \201 cation within the tumor may also be identi \201 ed. CT Usually a well-circumscribed hyperdense, mass seen on NCCT, that has a broad based attac hment to the dura. They enhance intensely following IV contrast. There is often internal ca lci \201 cation and hyperostosis of the adjacent bone. MRI (Fig. On T1 images the lesion will be either low signal or isointense and on T2 will be either isointense or high signal. There is avid contrast enhancement with the administrati on of gadolinium. Classically a \200\230dural tail \200\231 sign will be seen. 10.9 ) Angiography Meningiomas are almost always supplied by the external carotid artery and very rarely by the internal carotid artery. A \200\230mother in law \200\231 blush is typical, i.e. contrast shows up early and stays late! There is often a sunburst appearance of the fe eding vessels. Information for the radiologist \200 Previous history of radiotherapy. \200 Does the pa tient have neuro \201 bromatosis? SUBASH KC/NMC-15TH/2014 MENINGIOMA 159 (a) (b) Fig. 10.9 a) Axial T1-weighted post gadolinium image. b) Coronal T1-weighted post gadoliniu m image. The arrows point to a well-de \201 ned enhancing lesion attached to the posterior border of the petrous bone consistent with a small meningioma. SUBASH KC/NMC-15TH/2014 160 CHAPTER 10 Neurology conditions Brain metastases This is one of the most feared complications of systemic cancer by many pa tients. Metastases are the most common of the intracranial neoplasms and 6 primary tumors a ccount for the majority of all brain metastases. These are: lung, breast, colon, renal, mel anoma, and choriocarcinoma. Clinical presentation Symptoms are either usually caused by a rise in intracranial pressure with symptoms such as nausea and vomiting, headache, and confusion, or by a focal destruct ion of neurons at the site of the metastasis producing limb weakness, seizures, visual defe cts, or speech disturbance. Approximately 2/3 of all brain metastases are symptomatic. Imaging Plain \201 lm These are rarely used but lytic or sclerotic lesions on a skull rad iograph may be seen if there is bone extension. The most common primary tumors to show this pattern are lung and breast. CT In almost all patients presenting with symptoms suggestive of brain metas- tases CT will be the \201 rst investigation. The typical appearance is of low attenuation areas on NCC T, often multiple and usually found at the gray/ white matter junction. After IV contrast t hey will usually enhance and more lesions may become apparent. MRI (Fig. If there is only one lesion visible on CT then MRI may be used to look for furthe r lesions in order to con \201 rm the diagnosis of metastatic disease. Multiple lesions wi th surrounding oedema are often seen. These are low signal on T1 and high signal on T2 imag ing. Surrounding oedema is usually low signal on T1 and high signal on T2 imaging. 10.10 ) Information for the radiologist Information about any history or cancer is helpful, even if the cancer was some time ago, it may still be relevant. SUBASH KC/NMC-15TH/2014 BRAIN METASTASES 161 (a) (b) Fig. 10.10 visual disturbance. a) Axial T2 image with extensive left occipital oedema with a complex lesion, posteriorly. Low-grade oedema on the contralateral side. b) Axial T1 post -gadolinium-enhanced image demonstrating heterogeneous enhancement of the lesion consistent with a metastasis. A 54-year-old patient with known breast carcinoma with right-sided SUBASH KC/NMC-15TH/2014 162 CHAPTER 10 Neurology conditions Pituitary adenoma Background Conditions involving the pituitary gland were \201 rst descr ibed in 1886 by a French neurologist who studied 2 patients with symptoms suggestive of acr omegaly. Pituitary adenomas are benign, slowly growing tumors arising from the anterior lob e of the pituitary gland or adenohypophysis. Most pituitary adenomas arise spontaneously but can also occur as part of the multiple endocrine neoplasia I (MEN I) syndrome. Clinical presentation Symptoms may be due to either a local pressure effect from the tumor itself on surrounding structures, or may be related to distant endocrine manifestations. A large proportion of patients present with visual symptoms due to compression of the optic n erves. Classi \201 cation The tumors are classi \201 ed according to size: a tumor <10mm is term ed a microadenoma and when > 10mm is termed a macroadenoma. The func- tioning tumors are th en also classi \201 ed according to which hormone they secrete. Prolactinoma This is the most common of the pituitary adenomas. In women presenting feature s include amenorrhoea, infertility, and galactorrhoea. In men symp- toms include impotence, low libido, and visual disturbance. Corticotrophic adenoma This is an ACTH-secreting tumor which causes Cushing \200\231s disea se in this case include weight gain, osteoporosis, muscle weakness, a \200\230buffalo- hum p \200\231 at the back of the neck, dryness and thinning of the skin. \200\224 symptoms Somatotrophic adenoma These tumors secrete growth hormone causing gigantism in children and acromegaly in adults. Gonadotropic cell adenoma These tumors are quite rare and secrete luteinizing hormone and f ollicle- stimulating hormone. Symptoms in this case include amenorrhoea and impotence. Thyrotrophic cell adenoma This tumor secretes thyroid-stimulating hormone and produces sign s and symptoms of thyrotoxicosis, such as heat intolerance, sweating, tachy- cardia, and we ight loss. This type of adenoma is often large and invasive. Imaging Plain \201 lm Skull radiographs are now relatively rare but occasionally signs of a pitui- tary adenoma such as enlargement of the sella and erosion of the clinoid processe s may be seen. These \201 ndings are however non-speci \201 c and unreliable! SUBASH KC/NMC-15TH/2014 PITUITARY ADENOMA 163 CT Microadenomas will usually be seen as a focal hypodensity seen on both non-contrast and contrast-enhanced CT. The adenoma may enhance but not as quickly as the surrounding normal pituitary tissue. Other \201 ndings include deviation of the pituitary stalk and erosion of the sella \202 oor. Macroadenomas have variable appearances but most are isoattenuating relative to the cortex on non-enhanced CT scans and show moderate enhancement on enhanced scans. MRI (Fig. Coronal T1 images are the most sensitive. Adenomas are usually seen as a focus of low signal on T1 images and a focus of high signal on T2 images. 10.11 ) (a) (b) Fig. 10.11 a) Sagittal T1-weighted MRI image demonstrating tumor in the pituitary fossa. b) Post-gadolinium enhanced coronal image shows uniform enhancement throughout. This proved t o be a prolactinoma. SUBASH KC/NMC-15TH/2014 164 CHAPTER 10 Neurology conditions Multiple sclerosis This is a demyelinating disease affecting the spinal cord and the brain. The characteristic lesions are called plaques. Multiple sclerosis (MS) usually affects you ng adults and is more common in females. There is no known de \201 nite cause for this and at the present time no curative treatment is available. Clinical presentation Due to the nature of the condition it can present with almost any neu rolog- ical sign or symptom and may progress to cognitive and physical disabilities. The di agnosis requires objective evidence of lesions disseminated in time and space (McDonald cri teria speci \201 c to MS. This is an electrical sensation that runs down the back when ben ding the neck. 1 ). Lhermitte \200\231s sign is characteristic but not Imaging Currently a combination of clinical, laboratory, and radiological tests are used to make the diagnosis. The only radiological investigation of routine value is MRI. MRI (Fig. This is the investigation of choice as no other modality can demonstrate the plaq ues. A combination of T1-weighted, FLAIR, and post-contrast (gadolinium) enhanced can be us ed to detect these. The whole of the brain and the spinal cord should be covered. 10.12 ) Classically plaques are seen in the corpus callosum, U- \201 bres, temporal lobes, brainstem, cerebellum, and the spinal cord. Temporal lobe involvement is hi ghly speci \201 c for MS. Plaques show low signal on T1-weighted, high signal on FLAIR, an d enhance post-gadolinium in the brain (after they have been present for a month). Dawson \200\231s \201 ngers are typical for MS \200\224 these are ovoid lesions running perpend icular to the ventricles secondary to in \202 ammation around penetrating venules. Information for the radiologist \200 Has the patient had any other neurological events? \200 What is their current neurological status? Reference WI , 1 McDonald A , Compston Edan G , et al. Recommended diagnostic criteria for multiple sclerosis: guidelines from the International Panel on the diagnosis of multiple sclerosis 50 ( 1 ): . Ann Neurol 2001 ; 121 \200\223 7 . SUBASH KC/NMC-15TH/2014 MULTIPLE SCLEROSIS 165 (a) (b) Fig. 10.12 oedema of the cord consistent with a plaque. b) Axial FLAIR image of the brain. This shows multiple periventricular plaques. a) T2-weighted axial MRI image from the upper cervical spine showing SUBASH KC/NMC-15TH/2014 166 CHAPTER 10 Neurology conditions Epilepsy Epilepsy is a common chronic neurological disorder characterized by the occurrence of at least 2 unprovoked seizures 24 hours apart. Seizures result from an abnormal paroxys mal discharge of cerebral cortical neurons. Classi \201 cation \200 Generalized seizures: Tonic \200\223clonic (grand mal). \200 Absence (petit mal). \200 Myoclonic (rare involu ntary muscle jerks). Partial seizures: Simple partial (no impairment of consciousness, e.g. Jacksonian seizures). \200 Complex p artial (with impairment of consciousness, e.g. temporal lobe epilepsy). Clinical presentation This depends on the location of seizure activity in the cortex as wel l as the extent and pattern of its propagation in the brain. Imaging Neuroimaging should not be routinely requested when a diagnosis of idi- opathic gen eralized epilepsy has been made clinically. CT This can be used to identify gross pathology if MRI is not available or is contraindicat ed. MRI This is the imaging investigation of choice in individuals with epilepsy, par- ticularl y in those: \200 Who develop epilepsy before the age of 2 years or in adulthood. \200 W ho have any suggestion of a focal onset on history, examination or electroencephalography (EEG). In whom seizures continue in spite of \201 rst-line medication. Routine brain MRI may well reveal an underlying cause, such as neoplasia. This should be pe rformed within 4 weeks of presentation (NICE epilepsy guidelines 1 ). The principal role of MRI in epilepsy however, is in the de \201 nition of structural abnormalities that underlie seizure activity. In patients with drug-resistant ep ilepsy, excision of such a lesion may be curative or may improve seizure control. MR spectroscopy is sometimes used to assess concentrations of cerebral metabolites and some neurotransmitters non-invasively. Scintigraphy This can be used as a further means of imaging in potentially preopera- tive M RI-negative cases. PET may provide data on regional cerebral blood \202 ow, glucose metab olism, and the binding of speci \201 c ligands to receptors. SUBASH KC/NMC-15TH/2014 EPILEPSY 167 Information for the radiologist \200 Symptoms and signs at presentation and current seizu re activity. \200 Response to medical treatment. \200 If surgery is being considered. (a) (b) Fig. 10.13 a) Axial contrast-enhance CT demonstrating a mixed attenuation lesion anterior l eft insula region. b) Coronal T1 post gadolinium image con \201 rming this high-grade tumo r with extensive oedema. A 30-year-old patient who presented with 3 seizures over a week. Reference 1 NICE . primary and secondary care The epilepsies: the diagnosis and management of the epilepsies in adults and children in . London : NICE , 2004 . SUBASH KC/NMC-15TH/2014 This page intentionally left blank SUBASH KC/NMC-15TH/2014 169 Chapter 11 Head and neck differential diagnosis Bare orbit 170 Orbital calci \201 cation 170 Absent or hypoplastic paranasal sinuses Opaci \201 cation of maxillary antrum Nasopharyngeal mass 170 170 170 SUBASH KC/NMC-15TH/2014 170 CHAPTER 11 Head and neck differential diagnosis Bare orbit \200 Neuro \201 bromatosis. \200 Metastatic disease. \200 Meningioma. Orbital calci \201 cation \200 Cataract. \200 Retinoblastoma. \200 Previous infectio n. \200 Meningioma. \200 Vascular calci \201 cation. Absent or hypoplastic paranasal sinuses \200 Congenital. \200 Down \200\231s syndrome. \200 Kartagener \200\231s syndrome. \200 Paget \200\231s disease. \200 Fibrous dyspla sia. Opaci \201 cation of maxillary antrum \200 Trauma. \200 Infection. \200 Malignancy. \200 Fibrous dysplasia. \200 Wegener \200\231s granulomatosis. \200 Dentigerous/mucou s retention cyst. Nasopharyngeal mass \200 Normal adenoids (esp. in children). \200 Mass lesions: Nasopharyngeal cancer. \200 Lymphoma. \200 Angio \201 broma. \200 Rhabdomyosarcoma. \200 Trauma. \200 Infection. SUBASH KC/NMC-15TH/2014 171 Chapter 12 Head and neck presenting syndromes Neck lumps 172 Hoarse voice 173 Dysphagia 174 SUBASH KC/NMC-15TH/2014 172 CHAPTER 12 Head and neck presenting syndromes Neck lumps Differential depends on position: \200 Super \201 cial (within skin): Lipoma. \200 Sebaceous cyst. Anterior triangle: Lymph nodes (reactive or malignant). \200 Branchial cleft cyst. \200 Carotid body tumor . \200 Aneurysm. \200 Vascular malformation. Midline: Thyroid mass. \200 Thyroglossal duct cyst. \200 Laryngocoele. \200 Dermoid cyst. \200 Submandibular: \200 Lymph node. \200 Salivary gland infection. \200 Salivary gl and tumor. \200 Sialolithiasis. \200 Posterior triangle: Commonly lymph nodes. \200 Cervical rib. \200 Pharyngeal pouch (rare). Imaging Ultrasound Usual \201 rst-line modality for assessment of palpable lumps, it allo ws accu- rate localization and characterization, as well as guiding biopsy if required. CT Useful in assessment of deeper structures, especially if infection and abscess formation are being considered. MRI Gives better soft tissue characterization than CT and should be used if suspecting meta static disease from a nasopharyngeal and oropharyngeal primary. Fluoroscopy Sialography (contrast injection in the salivary gland ducts) gives accurate ima ges of the glandular structure, as well as stones or strictures in the duct. Nuclear medicine PET-CT is used in the assessment of malignant lymph nodes with no known pr imary. Scintigraphy is also used in cases of thyroid and parathy- roid enlargement. SUBASH KC/NMC-15TH/2014 HOARSE VOICE 173 Hoarse voice The commonest causes of a sudden change in voice quality are infection, laryng itis, pharyngitis, and epiglottitis. Imaging plays a role in cases where direct inspection raises the possibility of tumors on the vocal cord, or recurrent laryngeal nerve palsy. The left recurrent laryngeal nerve passes into the mediastinum and