MRI follow up. (B) April 2018: FLAIR sequences showed an extension of the white matter (WM) hyperintensity (B1, B2, B3); gradient-echo sequences showed microbleeds (B4, B5).


MRI follow up. (C) June 2018: FLAIR sequences showed a reduction of the WM alterations (C1, C2, C3); susceptibility-weighted imaging (SWI) sequences confirmed microbleeds (C4, C5).


MRI follow up. (D) February 2019: FLAIR sequences showed a further reduction of the WM alterations (D1, D2, D3); SWI sequences corroborated microbleeds (D4, D5).


Brain magnetic resonance imaging results. T2-weighted magnetic resonance imaging (axial image of the pons at the level of the medial longitudinal fasciculus) was normal in this patient.


Results of the L-DOPA test. One ground L-DOPA 100 mg/carbidopa 10 mg tablet was administered orally on an empty stomach after waking in the morning, and the L-DOPA blood concentration was measured seven times from before the tablet was administered to 240 min after ingestion. Prior to rehabilitative intervention, the tablet was ineffective (a "no-on" state), parkinsonian signs did not improve, and the maximum blood L-DOPA concentration was 0.78 nmol/mL (solid line). After dysphagia rehabilitation, the patient was able to swallow the tablets quickly, his parkinsonism symptoms improved within 30 min after administration, and his maximum blood L-DOPA concentration was 9.99 nmol/mL (dashed line).


The VNS device and an intraoperative photograph of the left vagosympathetic trunk. The pulse generator (width 45 mm, height 32 mm, depth 6.9 mm, and weight 16 g) (A).


The VNS device and an intraoperative photograph of the left vagosympathetic trunk. The electrode (B).


The VNS device and an intraoperative photograph of the left vagosympathetic trunk. The left vagosympathetic trunk wrapped by the two helical electrodes and anchor tether (C). VNS, vagus nerve stimulation.


The number of FS-GTCS and FS-GTCS clusters per month (A).


The number of FS and FS clusters per month (B).


The number of seizure days (FS-GTCS and FS) per month (C). The asterisk indicates that VNS therapy was initiated in this month. Months -5 to 0 indicate the retrospective period; months 1 to 12 indicate the follow-up period. FS-GTCS, focal seizures evolving into generalized tonic-clonic seizures; VNS, vagus nerve stimulation.


Magnetic resonance imaging of lumbosacral spine taken on the day of injury showing traumatic L3-L4 disc protrusion. L5 vertebra is sacralized.


Magnetic resonance imaging of lumbosacral spine taken after 4 months of index surgery showing recurrent disc protrusion L3-L4 with L4-L5 disc protrusion.


Patient is positioned prone toHall's frame with adequate padding for nipples and anterior superior iliac spines. Lumbar lordosis has been obliterated. Head is supported with pillows and head ring.


This picture shows discoloration and edema in the eyelids and periorbital region on the left eye.


Pictures of optical coherence tomography recording- subretinal fluid and optic disc edema in the region of a crowded optic nerve head with a low cup:disc ratio lead to a compromise in the microvasculature resulting in posterior ischemic optic neuropathy.


Axial sagittal computed tomography with brain.


Bone. Windows showing a small cutaneous mass over the previous craniotomy site with an underlying bony erosion and a small right frontal intracranial component (2016 study).


Front and top view of the patient's head showing the external appearance of the cutaneous meningioma with large lateral extension and disfigurement. There are multiple scalp ulcerations.


(a-c) Axial magnetic resonance imaging with contrast from the vertex till the basal ganglia showing significant intracranial component with bilateral frontal dural attachment and severe mass effect on the frontal lobes and lateral ventricles bilaterally.


The right superomedial invasion of the orbital cavity is appreciated (d).


(a-c) Sagittal magnetic resonance imaging with contrast showing the anterior and inferior extent of the cutaneous component with the involvement of the face and right orbit.


Coronal magnetic resonance imaging with contrast showing the lateral extent of the cutaneous component (a).


Magnetic resonance venography showing complete occlusion of the anterior and middle thirds of the superior sagittal sinus (b).


Axial T2 image showing the vasogenic edema surrounding the intracranial component (c).


His appearance from the side.


His appearance from the front.


Collapse of the stent proximal end and management. (A,B) Withdrawal of the micro-guidewire and microcatheter led to collapse of the stent proximal end with the stent proximal markers in close contact, and the blood flow was reduced through the proximal end. The longer arrow indicates the proximal markers and the shorter arrow the distal markers.


Collapse of the stent proximal end and management. (C) A 300-cm micro-guidewire was navigated into the stent lumen through the proximal lateral stent mesh rather than through the proximal stent end. The longer arrow indicates the collapsed proximal markers of the stent, whereas the double arrows indicate the micro-guidewire through the stent lateral mesh.


Collapse of the stent proximal end and management. After the micro-guidewire was sent to the distal segment of the basilar artery,. Is the local enlargement of. Between the proximal and distal markers of stent.


Collapse of the stent proximal end and management. After the micro-guidewire was sent to the distal segment of the basilar artery,. The proximal stent end was opened with the proximal markers being spread out [, shorter arrow]. The longer arrow indicates the distal stent markers.


Collapse of the stent proximal end and management. (F) A second 200-cm micro-guidewire was sent right through the opened proximal stent end into the stent lumen (double arrows).


Follow-up angiography at 6 months after stenting demonstrates unobstructed blood flow through the stented vertebral artery (A,B) with no stenosis.


Anti-NMDA receptor antibodies in patient's cerebrospinal fluid and serum. Anti-NMDA receptor antibodies were positive in cerebrospinal fluid (IgG, 1:32) ,serum (IgG.


Anti-NMDA receptor antibodies in patient's cerebrospinal fluid and serum. 1:320). Before immunotherapy.


Anti-NMDA receptor antibodies in patient's cerebrospinal fluid and serum. 1:32). After 5 months of immunotherapy. . Abbreviation: NMDA, N-methyl-D-aspartate.


(a) FLAIR magnetic resonance imaging showing right temporal and insular lesion with right to left mass effect and surrounding edema.


(b and c) CT with contrast demonstrating irregular enhancement of a large right temporal and insular lesion.


(d) A coronal view of the preoperative CT with contrast, with an emphasis on the Sylvian fissure and middle cerebral artery (MCA) being pushed upward (asterisk).


(a) Postoperative CT with minimal hemorrhage in the posterior aspect of the resection cavity.


(b) The T1 magnetic resonance imaging (MRI) with contrast respectively, with small amount of residual tumor anterosuperiorly and medially, with small amount of hemorrhage within the resection cavity and no evidence of hemorrhage within the basal cisterns.


(c) Diffusion-weighted imaging without any evidence of infarct.


(d) A T2 MRI with hypointensities along exposed middle cerebral artery (asterisks), representing Gliadel wafer lining the vessel and cavity.


Pathological findings. Brain biopsy from the left frontal lobe. (A) Hematoxylin and eosin staining.


Pathological findings. Brain biopsy from the left frontal lobe. (B) CD20 immunohistochemical staining.


Pathological findings. Brain biopsy from the left frontal lobe. (C) Ki-67 immunohistochemical staining.


Pathological findings. Brain biopsy from the left frontal lobe. (D) CD3 immunohistochemical staining.


Contrast-enhanced brain MRI recorded 1 month after brain biopsy shows a spotty gadolinium enhancement in the left periventricular white matter (arrow) and post-biopsy scar (arrowhead).


With T2 hyperintensities.


(C) This lesion does not show abnormal hyperintensities on diffusion-weighted imaging (DWI).


Primary gaze showing right exotropia and left hypotropia with head tilt to left.


Mobile larvae completely obstructing left external ear canal.


Appearance of live larvae.


Fluid attenuation inversion recovery magnetic resonance image showing a hyperintense lesion in the right parietal area.


Interictal scalp electroencephalography indicating repetitive spikes in the parietal area.


Patient transverse T2 magnetic resonance imaging results. The swallow-tail sign (red arrow) was absent.


Patient single-photon emission computed tomography images. There was asymmetrical uptake in the caudate nucleus (white arrows).


Test for attentional performance.


Fundus photographs at the initial visit in a 15-year-old boy with AMN. There are no specific abnormalities in the right eye (a).


Fundus photographs at the initial visit in a 15-year-old boy with AMN. There is a slightly darker area in the fovea of the left eye (b).


Anteroposterior and lateral radiograph of the right leg showing lytic lesion with large soft-tissue component and hair-on-end periosteal reaction in mid-diaphysis of tibia.


Left eye. Total ptosis.


Left eye. Total ophthalmoplegia.


(a) H and E-stained section of nasopharyngeal punch biopsy specimen showing nests of small round blue cells, (b) Strong CD99 immunoreactivity.


Brain CT scan before extraction of ventriculoperitoneal shunt.


Brain CT scan after extraction of ventriculoperitoneal shunt, there was no changes in hydrocephalus.


Ictal epileptic headache during NCSE documented by video-EEG. The EEG tracing showed the activation of subcontinuous epileptic activity consisting of GSWDs, clinically related to a prolonged tensive headache with bilateral and symmetrical eyelid flutter (a).


Ictal epileptic headache during NCSE documented by video-EEG. The EEG pattern confirmed the presence of an eye closure sensitivity characterized by GSWDs related to bilateral and symmetrical eyelid flutter (b).


Video-EEG performed some days after NCSE, showing a normal tracing during rest.


During eye closure.


(a) Clinical photograph showing left eye ptosis.


(b) Clinical photograph showing normal sized pupils.


NCCT Head showing diffuse sub arachnoid hemorrhage in the basal cisterns.


CT Angiography cerebral vessels showing ACom aneurysm.


Genetic family diagram of the patient.


MRI (magnetic resonance imaging) after bSCG-DBS implantation (the red circle is STN, and the blue circle is GPi).


(A) Trends in UPDRS-III off-period scores.


(B) Trends in UPDRS-III on-period scores.


(C) Trends in UPDRS-IV scores.


(D) Trends in NMSS scores.


(E) Trend in PDQ-39 scores.


(F) Trends in Levodopa Equivalents (LDE).


(G) Comparison of UPDRS-III score in 4 conditions (pre-surgery, GPi stimulation, STN stimulation, and combined GPi and STN stimulation).


(H) Comparison of UPDRS-IV score in 4 conditions (pre-surgery, GPi stimulation, STN stimulation, and combined GPi and STN stimulation).


Facial appearance of the patient at the age of 16. Note brilliant blue irides, hypertelorism, dystopia canthorum, hirsutism.


Magnetic resonance imaging (MRI) of the patient. (A) Shown is the preoperative MRI of the 2; 10 year old patient.


Magnetic resonance imaging (MRI) of the patient. (B) Normal MRI of the patient 6 months after surgery showing the malacic transformed medial infarct on the right side with no evidence of hemorrhage, infarction, or liquor circulatory disturbances.


Electroencephalogram (EEG) of the patient. (A) Awake EEG after hemispherotomy under VPA. Hypersynchronous activity on the right frontocentral side over the disconnected hemisphere without evidence of clinical seizure signs and without evidence of transition to the left.


Electroencephalogram (EEG) of the patient. (B) Six months after surgery without VPA, the EEG showed continuous right hemispheric dysfunction, hypersynchronic right frontocentral activity, and activation during sleep without clinical signs.


(A) The MEG ECD method delineated epileptic zone at right posterior cingulate cortex.


(B) The MEG STOUT method delineated epileptic zone at the left insular long gyrus of island and the parietal opercula. Thirteen spikes were marked in this patient and Source localization was conducted using ECD and STOUT on each spike within a -100 to 100 ms time window around the peak spike signal. All results displayed over the corticalsur face are thresholded at 50% of the maximum amplitude. As ECD method assumes that a small number of focal sources exist that can be equivalent to a few current dipoles in the brain, the result of MEG ECD method is localized to right posterior cingulate cortex. And the STOUT method is localized to the left insular long gyrus of island and the parietal opercula through localization bias compensation.


(C) The position of eight intracranial electrodes.


Previous MRI (a) High-resolution T2 MRI showing cerebral aqueduct stenosis/web.


(b) Axial FLAIR MRI showing abnormal signal in the optic chiasm extending to bilateral optic tracts and in the midbrain from the interpeduncular fossa extending between the red nuclei to the area of the oculomotor nuclei.


Preshunt adjustment axial T1 MRI demonstrating slit ventricles suggestive of shunt overdrainage.


Preshunt adjustment sagittal T2 MRI showing normal 4th ventricle and cistern spaces, no distortion of brainstem or splenium and no tonsillar herniation.


Five months postshunt adjustment looking straight ahead with no downward gaze preference, strabismus or ptosis. Subtle horizontal divergence.


Five months postshunt adjustment looking down. Left eye deviation laterally.


Five months postshunt adjustment attempting to look upward. Persistent upgaze limitation with lateral deviation of the left eye.


Right temporal lobe biopsy. HE staining. Magnification is x40. Mildly hypercellular and gliotic gray matter with focal reactive changes. No neoplasia is seen.


Brain magnetic resonance imaging demonstrating characteristic findings of stroke-like migraine attacks after radiation therapy syndrome. Fluid-attenuated inversion recovery image demonstrates insular, and ,temporal T2 hyperintensities near the site of prior radiated tumor.


Brain magnetic resonance imaging demonstrating characteristic findings of stroke-like migraine attacks after radiation therapy syndrome. With corresponding gyriform enhancement on postcontrast T1-weighted axial image.


Brain magnetic resonance imaging demonstrating characteristic findings of stroke-like migraine attacks after radiation therapy syndrome. Expected lack of abnormalities noted on diffusion-weighted.


Brain magnetic resonance imaging demonstrating characteristic findings of stroke-like migraine attacks after radiation therapy syndrome. Perfusion. Images.


Brain magnetic resonance imaging demonstrating characteristic findings of stroke-like migraine attacks after radiation therapy syndrome. Posttherapy imaging at 10 days demonstrates improved signal abnormalities on. Fluid-attenuated inversion recovery.


Brain magnetic resonance imaging demonstrating characteristic findings of stroke-like migraine attacks after radiation therapy syndrome. Reduced enhancement on. Postcontrast T1-weighted sequences.


MRI scan sections of the patient's brain reporting the presence of GMH (indicated by arrows and circles). T2W - coronal section.


MRI scan sections of the patient's brain reporting the presence of GMH (indicated by arrows and circles). T1W- assial section.


MRI scan sections of the patient's brain reporting the presence of GMH (indicated by arrows and circles). T1W - sagittal section. Arrows indicate areas of subependimal alterated signal (bilateral and asymmetrical PNH:Periventricular Nodular Heterotopia:with heterotopic grey matter stretching all along the ventricular walls, maximum diameter = 5 mm). Note that the shade of grey is the same as that of the cortical grey matter (the same signal intensity), which confirms that it is grey matter:the pathognomonic finding in GMH.


Brain magnetic resonance imaging (MRI):Rheumatoid meningitis. (A) Axial T1-weighted sequence post-gadolinium shows faint contrast enhancement of the leptomeninges and underlying gyri over the left convexity.


Brain magnetic resonance imaging (MRI):Rheumatoid meningitis. (B) Finite areas of diffusion restriction of the left parietal cortex near the vertex on axial diffusion weighted imaging (DWI) sequence.


Brain magnetic resonance imaging (MRI):Rheumatoid meningitis. (C) Coronal T1-weighted sequence post-gadolinium shows longitudinal right frontal leptomeningeal and faint left leptomeningeal contrast enhancement.


Brain magnetic resonance imaging (MRI):Rheumatoid meningitis. (D) Axial DWI sequence shows new areas of restricted diffusion in the right frontal parafalcine region along with increased volume of restricted diffusion in left parietal cortex near the vertex.


Brain magnetic resonance imaging (MRI):Rheumatoid meningitis. (E) Axial T1-weighted sequence post-gadolinium obtained 3 months following immunosuppressive therapy showing no abnormal contrast enhancement, and left frontal postoperative changes.


Brain magnetic resonance imaging (MRI):Rheumatoid meningitis. (F) Axial DWI sequence obtained 3 months following immunosuppressive therapy and demonstrating the resolution of previously documented findings.


Meningeal histologic sections:Rheumatoid meningitis. Representative hematoxylin and eosin (H&E) stained sections. (A) Meningothelial hyperplasia (magnification 200).


Meningeal histologic sections:Rheumatoid meningitis. Representative hematoxylin and eosin (H&E) stained sections. (B) Necrobiotic core surrounded by palisading macrophages (magnification 200).


Meningeal histologic sections:Rheumatoid meningitis. Representative hematoxylin and eosin (H&E) stained sections. (C) Cluster of inflammatory infiltrate cells consisting mainly in small lymphocytes, mixed with few plasma cells and histiocytic cells (magnification 400).


Meningeal histologic sections:Rheumatoid meningitis. Representative hematoxylin and eosin (H&E) stained sections. (D) Diffuse meningeal inflammatory infiltrate (magnification 400).


(A) Seizure with a left frontotemporal focus. Ictal electroencephalography (EEG) showed rhythmic and reluctant fast (12-13 Hz) activity primarily involving the left frontotemporal area consisting of polyspikes of about 100 mV amplitude with reversal phase in the F7 lead, then epileptic discharge involved all channels and showed a reduction in frequency (6 Hz). The patient was unconscious. Discharges consisting of high-amplitude sharp waves (90-100 muV) and slow waves (prominent on the frontotemporal areas) (high 30 Hz, low 0.1 second; rate 15 mm/second).


(B) EEG during pseudoseizures. Normal background activity with interictal abnormalities in left frontocentrotemporal channels: sporadic and nonperiodic sharp waves at 100 mV with reversal phase on F7 and sporadic anterior synchronous and asynchronous theta activity (6-7 Hz, 50-60 mV). Muscular artifacts on right frontal derivations and two abrupt movement artifacts were concomitant with fictitious spasms of the patient. No epileptic seizures were recorded. This recording showed a significant reduction of interictal activity in comparison with her previous EEGs.


(a) EKG on admission. Notice the isolated ST-T segment elevation in V2.


(b) Patient's baseline normal EKG obtained a few months prior to admission.


(c) Left ventriculogram-end diastole.


(d) Left ventriculogram-end systole. Notice the severe hypokinesia to akinesia in the anteroapical area and balloon-like dilation of the LV apex during systole.


(a) Pressure tracing during pull back from left ventricle to LVOT. Notice the progressive drop of pressure.


(b) Pressure tracing from LVOT to aorta.


(c) TEE with color Doppler during systole. Notice the severe MR jet from LV to LA.


(d) Systolic anterior motion (SAM) of the anterior mitral valve leaflet. Positions of both leaflets during systole are outlined. Arrow pointing to the anterior leaflet.


Fundus photograph and OCT image of a patient with nAMD in the right eye. A; Fundus photograph before the first intravitreal ranibizumab injection showing normal optic disc cupping.


Fundus photograph and OCT image of a patient with nAMD in the right eye. B; OCT image showing the presence of CNV and SRF.


Fundus photograph and OCT image of the same patient with nAMD. A; Fundus photograph at 4 weeks after the 25th intravitreal ranibizumab injection, and before the first intravitreal aflibercept injection showing the presence of hard exudates.


Fundus photograph and OCT image of the same patient with nAMD. B; OCT image showing the residual SRF and retinal edema.


Fundus photograph and OCT image of the same patient with nAMD. A; Fundus photograph after trabeculotomy, demonstrating the absence of hard exudates.


Fundus photograph and OCT image of the same patient with nAMD. B; OCT image after trabeculotomy showing that both the SRF and the retinal edema have completely disappeared.


Multiple tense bullae-clinical aspect of bullous pemphigoid.


Erythematous plaques covered with tense blisters with clear fluid-clinical aspect of bullous pemphigoid.


Erythematous scaly plaques-clinical aspect of psoriasis vulgaris.


Atrophic epidermis with sub-epidermal blister containing numerous eosinophils and neutrophils, col. HE x 40.


Atrophic epidermis with sub-epidermal blister containing numerous eosinophils and neutrophils, col. HE x 100.


Atrophic epidermis with sub-epidermal blister containing numerous eosinophils and neutrophils, col. HE x 200.


MRI performed 10 days after onset of the second prolonged attack. Right temporal-occipital hyperintensity on T1-weighted images.


MRI performed 10 days after onset of the second prolonged attack. With gliosis on T2-FLAIR images. Suggests the chronic stage of cortical necrosis caused by first prolonged attack. Left temporal-occipital cortex hyperintensity on T2-FLAIR images.


MRI performed 10 days after onset of the second prolonged attack. With gyriform enhancement.


MRI performed 10 days after onset of the second prolonged attack. Restricted diffusion.


MRI performed 10 days after onset of the second prolonged attack. Normal apparent diffusion coefficient (ADC). Suggests the subacute stage of cortical necrosis caused by second prolonged attack.


MRI performed 10 days after onset of the second prolonged attack. MRA demonstrated vasodilation of the branches of the left middle cerebral artery (MCA) and posterior cerebral artery (PCA) (F).


MRI performed 15 days after the onset of the second prolonged attack. DWI showed extensive cortical edema with diffusion restriction involving the left hemisphere (a).


MRI performed 15 days after the onset of the second prolonged attack. T1-weighted images showed slight hyperintensity in left temporal-occipital lobe and volume loss of right temporal-occipital lobe, suggestive of subacute and chronic stage of cortical necrosis, respectively (b).


MRI performed 15 days after the onset of the second prolonged attack. Gadolinium-enhanced T1-weighted images showed cortical enhancement in the left temporal-occipital lobe (c).


MRI performed 15 days after the onset of the second prolonged attack. MRA showed dilation of left MCA and PCA (d).


MRI performed 15 days after the onset of the second prolonged attack. PWI showed increased cerebral blood flow (CBF).


MRI performed 15 days after the onset of the second prolonged attack. Cerebral blood volume (CBV). In the left hemisphere. Region of interest (ROI) placed on the left temporal-parietal area showed a mean relative CBF value of 486.1 compared with that of 123.1 on the right temporal-parietal area. ROI placed on the left temporal-parietal area showed a mean relative CBV value of 533.1 compared with that of 129.8 on the right temporal-parietal area.